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Arterial Blood Gas (ABG) Interpretation: A Step-by-Step Emergency Guide

Why this matters: ABGs show how well a patient is oxygenating, ventilating and controlling acid–base balance. They help the emergency team recognise respiratory failure, shock, diabetic ketoacidosis, sepsis, poisoning and ventilator problems. Interpretation is not a number game: always match the gas with the patient, treatment, oxygen delivery and trend.

Scope and safety: Arterial puncture and analyser use require training, PPE and local policy. If a patient is crashing, treat airway, breathing and circulation first. Never delay oxygenation, ventilation, CPR, antidote or sepsis care while waiting for a gas.

Learning outcomes

Explain pH, PaCO2, PaO2, HCO3−, base excess, lactate and oxygen saturation.
Use a repeatable six-step approach to identify primary respiratory/metabolic disorders and compensation.
Calculate anion gap and recognise high-gap, normal-gap and mixed metabolic acidosis.
Assess oxygenation, A–a considerations, ventilator response and clinical urgency.
Recognise sampling errors and communicate a concise, actionable ABG handover.

1. What an ABG measures

Parameter	Typical adult reference (lab dependent)	Meaning
pH	7.35–7.45	Overall acidity/alkalinity. Acidaemia is below 7.35; alkalaemia is above 7.45.
PaCO2	35–45 mmHg (4.7–6.0 kPa)	Respiratory component; rises with hypoventilation and falls with hyperventilation.
HCO3−	22–26 mmol/L	Metabolic/renal component; calculated on many analysers.
PaO2	Usually about 80–100 mmHg on room air at sea level	Dissolved oxygen; interpret with FiO2, altitude, age and clinical context.
SaO2	About 95–100% in healthy adults	Percentage of haemoglobin carrying oxygen; compare with pulse oximetry.
Base excess (BE)	−2 to +2 mmol/L	Estimate of metabolic acid/base component; negative suggests metabolic acidosis, positive metabolic alkalosis.
Lactate	Often <2 mmol/L (lab dependent)	Marker of anaerobic metabolism/stress; trend is more useful than one isolated value.

2. Safe sampling and pre-analytical quality

Confirm patient identity, indication, oxygen device/flow or FiO2, ventilator settings and time of sample.
Explain the procedure, check Allen/collateral circulation according to policy and use PPE.
Use a heparinised syringe, avoid excess liquid heparin, remove air bubbles and mix gently.
Apply firm pressure after radial puncture—longer if anticoagulated or bleeding risk is present.
Send promptly at the temperature/time specified by the laboratory; delays alter PaO2, PaCO2 and pH.
Label the sample and record body temperature, oxygen therapy, ventilator settings, position and clinical events.

Common errors: Air bubbles can falsely raise PaO2 or lower PaCO2; venous blood is not interchangeable with arterial blood for oxygenation; excessive liquid heparin dilutes results; prolonged transport allows cells to consume oxygen and produce CO2.

3. The six-step ABG method

Check the patient and sample: identity, oxygen/ventilator settings, temperature and timing.
Look at pH: acid, normal or alkaline? A normal pH can hide a mixed disorder.
Identify the primary process: PaCO2 changes in the opposite direction to pH for respiratory disorders; HCO3− changes in the same direction as pH for metabolic disorders.
Check compensation: is the second value changing as expected, or is a second primary disorder present?
Assess oxygenation and lactate: PaO2/SaO2 relative to FiO2, A–a context and perfusion.
Integrate and act: diagnose the likely cause, treat the patient and repeat the gas after a meaningful intervention.

“pH → CO2/HCO3 → compensation → oxygen → cause → trend.” Repeat this order for every gas until it becomes automatic.

4. Primary acid–base disorders

Disorder	pH	Primary change	Common causes
Respiratory acidosis	Low	PaCO2 high	Opioids/sedatives, COPD exacerbation, severe asthma fatigue, neuromuscular weakness, CNS depression.
Respiratory alkalosis	High	PaCO2 low	Pain/anxiety, sepsis, pregnancy, hypoxia, pulmonary embolism, excessive ventilation.
Metabolic acidosis	Low	HCO3− low/BE negative	Lactic acidosis, DKA, renal failure, diarrhoea, toxins, sepsis and shock.
Metabolic alkalosis	High	HCO3− high/BE positive	Vomiting, gastric suction, diuretics, mineralocorticoid excess, hypokalaemia.

5. Compensation: is the response appropriate?

Compensation moves pH toward normal but does not usually return it completely to normal. If the compensation is more or less than expected, suspect a mixed disorder. Use your local calculator/formula and clinical judgement.

Primary disorder	Useful bedside rule	Interpretation
Metabolic acidosis	Winter’s formula: expected PaCO2 ≈ 1.5 × HCO3− + 8 ± 2.	Higher PaCO2 suggests additional respiratory acidosis; lower suggests additional respiratory alkalosis.
Metabolic alkalosis	PaCO2 usually rises about 0.7 mmHg for each 1 mmol/L rise in HCO3− (with limits).	Less rise suggests respiratory alkalosis; excessive rise suggests respiratory acidosis.
Respiratory acidosis	Acute HCO3− rises about 1 mmol/L per 10 mmHg PaCO2 rise; chronic about 3–4.	Small bicarbonate rise = acute; larger rise = renal/chronic compensation.
Respiratory alkalosis	Acute HCO3− falls about 2 mmol/L per 10 mmHg PaCO2 fall; chronic about 4–5.	More/less change than expected suggests mixed disease.

6. Anion gap and metabolic acidosis

The anion gap estimates unmeasured anions: AG = Na+ − (Cl− + HCO3−). A typical reference is about 8–12 mmol/L without potassium, but use the local laboratory range. Correct for low albumin because hypoalbuminaemia can hide a high-gap acidosis.

Pattern	Causes	EMT/emergency clue
High anion-gap metabolic acidosis	Lactic acidosis, ketoacidosis, renal failure, methanol, ethylene glycol, salicylates and other toxins.	Search for shock/sepsis, diabetes, renal disease, alcohol/starvation and poisoning.
Normal anion-gap (hyperchloraemic) acidosis	Diarrhoea, renal tubular acidosis, large chloride-fluid load, urinary diversions.	History of GI loss/fluids and potassium disturbance helps.
High-gap + high HCO3− gap	Possible additional metabolic alkalosis (e.g., vomiting) or chronic respiratory acidosis.	Do not treat a “normal” pH without identifying the mixed process.

Delta ratio: compare the rise in anion gap with the fall in bicarbonate when evaluating a high-gap acidosis. A much larger or smaller change suggests an additional metabolic disorder; use this as a prompt for expert review, not a standalone diagnosis.

7. Oxygenation interpretation

Read PaO2 together with FiO2, oxygen device, altitude, haemoglobin, SpO2 and work of breathing.
A PaO2 that seems “normal” on a high FiO2 may represent severe gas-exchange failure.
PaO2 may be falsely high after air contamination; carbon monoxide can give a misleadingly normal PaO2 and pulse oximeter.
Use the P/F ratio (PaO2 ÷ FiO2) in critical care discussions, but let the ICU team apply ARDS definitions and ventilator changes.
Low PaO2 with normal/high PaCO2 and fatigue is an emergency: support oxygenation and ventilation while treating the cause.

8. Worked emergency patterns

ABG pattern	Likely interpretation	Clinical action
pH 7.22, PaCO2 60, HCO3− 24	Acute respiratory acidosis.	Assess airway/ventilation, opioids or sedatives, fatigue and COPD/asthma; support ventilation and repeat after intervention.
pH 7.28, PaCO2 25, HCO3− 12	Metabolic acidosis with respiratory compensation; check Winter’s expected PaCO2.	Search for lactate, DKA, renal failure, diarrhoea and toxins; treat shock and the cause.
pH 7.50, PaCO2 28, HCO3− 22	Acute respiratory alkalosis.	Look for hypoxia, pulmonary embolism, sepsis, pain, pregnancy or excessive ventilator rate.
pH 7.52, PaCO2 48, HCO3− 38	Metabolic alkalosis with respiratory compensation.	Ask about vomiting, gastric suction, diuretics, chloride depletion and hypokalaemia.
pH 7.36, PaCO2 60, HCO3− 33	Compensated/chronic respiratory acidosis, or mixed process if clinically acute.	Compare baseline, assess COPD/neuromuscular disease and do not “normalise” chronic CO2 without expert guidance.
pH 7.40, PaCO2 20, HCO3− 12	Mixed respiratory alkalosis and metabolic acidosis can create a deceptively normal pH.	Consider sepsis, salicylates, liver failure or pregnancy; escalate urgently.

9. Clinical causes linked to ABG patterns

Emergency	Expected clues	Priority
Opioid/sedative overdose	Respiratory acidosis, low respiratory rate, reduced consciousness, small pupils.	Airway/ventilation, glucose, naloxone when indicated and observation for recurrence.
DKA	High-gap metabolic acidosis, low HCO3−, Kussmaul breathing, hyperglycaemia/ketones.	Fluids, potassium/insulin protocol and search for infection; do not stop compensatory breathing unnecessarily.
Sepsis/shock	Lactic acidosis, rising lactate, low pH, hypotension or abnormal perfusion.	Oxygenation, fluids/vasopressor pathway, antibiotics/source control and serial lactate.
COPD exacerbation	High PaCO2, variable pH, chronic bicarbonate elevation; hypoxaemia.	Titrate oxygen, bronchodilator/NIV protocol, assess fatigue and avoid harmful over-ventilation.
Salicylate poisoning	Respiratory alkalosis plus high-gap metabolic acidosis, tinnitus, vomiting, altered state.	Poison-centre advice, avoid respiratory suppression and arrange urgent toxicology care.
Pulmonary embolism	Low PaCO2, respiratory alkalosis, hypoxaemia or normal PaO2 early.	Do not dismiss as panic; urgent assessment and haemodynamic support.
Severe asthma	Early low PaCO2, later normal/rising PaCO2 with exhaustion—a dangerous sign.	Escalate immediately; prepare ventilation and treat bronchospasm.

10. ABG and mechanical ventilation

Rising PaCO2 with falling pH may indicate inadequate minute ventilation, increased dead space, fatigue, obstruction or circuit/ventilator failure.
Falling PaO2 despite increasing FiO2 suggests shunt, alveolar collapse, pneumonia, oedema, pneumothorax, tube displacement or inadequate PEEP.
A sudden ETCO2 change often precedes or accompanies ABG change; correlate both rather than chasing isolated numbers.
After a ventilator change, allow an appropriate time for equilibration and repeat gas based on urgency; never make multiple undocumented changes.

11. Clinical scenarios

Scenario 1 — DKA with fatigue: A young patient has pH 7.18, HCO3− 10 and PaCO2 24 with deep breathing. The low PaCO2 is compensation. Do not sedate or suppress breathing; treat DKA/shock urgently and watch for fatigue and cerebral deterioration.

Scenario 2 — Opioid overdose: A patient is drowsy with RR 6, pH 7.20, PaCO2 70 and HCO3− 27. This is acute respiratory acidosis. Open/assist the airway, ventilate, give naloxone if indicated and repeat assessment rather than relying on oxygen alone.

Scenario 3 — Sepsis: pH 7.30, HCO3− 15, PaCO2 30 and lactate 6 indicate metabolic acidosis with respiratory compensation. Look for infection, poor perfusion and rising work of breathing; begin sepsis care and serial reassessment.

Scenario 4 — Salicylate exposure: pH 7.45, PaCO2 20 and HCO3− 14 may look “normal” overall but represent mixed respiratory alkalosis and metabolic acidosis. Ask about aspirin, tinnitus and vomiting and call toxicology urgently.

Scenario 5 — Ventilator deterioration: A ventilated patient’s PaCO2 rises from 42 to 70 with falling pH and high airway pressure. Assess the patient and DOPE: tube displacement, obstruction/secretions, pneumothorax or equipment failure before changing settings.

12. ABG interpretation and handover template

State patient, indication, oxygen device/FiO2, ventilator mode/settings and time of sample.
Report pH, PaCO2, HCO3−, BE, PaO2/SaO2, lactate and key electrolytes.
Give the primary disorder, compensation status and any mixed disorder.
Describe clinical correlation: respiratory rate/effort, perfusion, mental state, glucose, temperature and trend.
State intervention already given, response and the specific concern/request to the receiving clinician.

13. When an ABG is urgent

Severe respiratory distress, altered consciousness, shock, cardiac arrest or suspected ventilatory failure.
Rapidly changing oxygen requirement, unexpected ventilator alarm or ETCO2 change.
Suspected DKA, sepsis/lactic acidosis, severe asthma/COPD, poisoning or metabolic crisis.
Persistent hypoxaemia despite oxygen, cyanosis, exhaustion or impending intubation.
Any gas that does not fit the patient—repeat/verify sample and escalate.

14. Revision questions

Which ABG values represent the respiratory and metabolic components?
How do you identify the primary process when the pH is abnormal?
What is Winter’s formula used for?
List five causes of high anion-gap metabolic acidosis.
Why can a normal pH hide a dangerous mixed disorder?
What does rising PaCO2 in a tired asthmatic patient signify?
How does FiO2 change interpretation of PaO2?
What sampling errors can produce misleading results?
Why should oxygenation and ventilation be treated before the final ABG diagnosis?
What information must accompany an ABG handover?

15. Key take-home points

Interpret pH first, then CO2/HCO3, compensation, oxygenation and the clinical cause.
Compensation should be appropriate; a normal pH does not exclude a mixed emergency.
Always interpret PaO2 with FiO2/oxygen device and trend, not as an isolated number.
High-gap metabolic acidosis demands a search for lactate, ketones, renal failure and toxins.
ABG supports decisions but never replaces ABCDE, examination and continuous reassessment.

Selected authoritative resources

For EMT practice: A gas is a snapshot of physiology. Read it in context, act on the life threat, repeat it after intervention and communicate the pattern—not just the numbers.

Arterial Blood Gas (ABG) Interpretation: A Step-by-Step Emergency Guide Read More »

Mechanical Ventilation: Modes, Settings, Alarms and EMT Safety

Why this matters: Mechanical ventilation supports patients who cannot maintain oxygenation, ventilation or airway protection. Emergency staff must understand why a patient is ventilated, what each setting does, how to recognise deterioration and how to safely move a ventilated patient between scene, ambulance, emergency department and ICU.

Scope and safety: Ventilator selection and settings are prescribed by trained clinicians and adjusted to the patient, disease and blood gases. Never alter a ventilator blindly. If a ventilated patient deteriorates, immediately assess the patient, manually ventilate with a self-inflating bag and oxygen if necessary, then troubleshoot the machine and circuit.

Learning outcomes

Explain the difference between oxygenation failure, ventilation failure and airway-protection failure.
Describe common invasive and non-invasive ventilation modes and the meaning of key settings.
Recognise high-pressure, low-pressure, apnoea, oxygen-supply and power alarms.
Apply lung-protective principles, patient–ventilator synchrony, humidification and infection prevention.
Use clinical assessment, SpO2, ETCO2 and ABG trends to judge response and escalation.
Prepare safe transport, handover, weaning readiness and emergency disconnection plans.

1. Why patients need ventilatory support

Indication	Examples	What ventilation must achieve
Oxygenation failure	Pneumonia, pulmonary oedema, ARDS, severe asthma/COPD, drowning.	Improve alveolar oxygen transfer while avoiding oxygen toxicity and pressure injury.
Ventilation failure	Opioid/sedative overdose, neuromuscular weakness, fatigue, severe hypercapnia.	Remove CO2 and correct respiratory acidosis without excessive minute ventilation.
Airway protection	Coma, seizures, severe facial trauma, shock or repeated vomiting.	Maintain a secure airway and prevent aspiration.
Work-of-breathing failure	Exhaustion, severe obstructive disease, chest wall restriction.	Reduce respiratory muscle load and allow recovery.
Raised intracranial pressure	Severe head injury, intracranial haemorrhage.	Prevent hypoxia and harmful hypo/hypercapnia while maintaining cerebral perfusion.

2. Key terminology

Term	Meaning	Clinical effect
Tidal volume (VT)	Volume delivered with each breath.	Too high increases volutrauma; too low may cause inadequate ventilation if not monitored.
Respiratory rate	Mandatory or total breaths per minute.	Changes minute ventilation and CO2 clearance.
Minute ventilation	VT × respiratory rate, adjusted by dead space.	Major determinant of PaCO2; excessive ventilation can cause alkalosis and lung injury.
FiO2	Fraction of inspired oxygen.	Corrects hypoxaemia; titrate to target rather than leaving high indefinitely.
PEEP	Positive pressure remaining at end-expiration.	Recruits alveoli and improves oxygenation but may reduce venous return and blood pressure.
Pressure support	Inspiratory assist for spontaneous breaths.	Reduces work of breathing during NIV or weaning.
Inspiratory time/flow	How quickly and how long gas enters the lungs.	Changes synchrony, air trapping and peak pressures.
Peak/plateau pressure	Peak reflects resistance; plateau approximates alveolar pressure.	High values suggest obstruction, secretions, poor compliance or overdistension.

3. Common ventilator modes

Mode	What the ventilator controls	Typical use/limitations
Volume-controlled assist/control	Set VT and rate; pressure varies with compliance/resistance.	Reliable minute volume; monitor peak/plateau pressure and auto-PEEP.
Pressure-controlled assist/control	Set inspiratory pressure and time; delivered VT varies.	Limits pressure; monitor exhaled VT and minute ventilation for changes in compliance.
SIMV	Mandatory breaths synchronised with patient plus spontaneous breaths.	May be used during transition; can increase work if poorly synchronised.
Pressure support ventilation	Patient triggers every breath; ventilator adds pressure.	Weaning or spontaneous breathing; unsafe in apnoea without backup.
CPAP	Continuous positive pressure during spontaneous breathing.	Recruits alveoli; requires alert/cooperative patient with protected airway.
NIV BiPAP	Different inspiratory and expiratory pressures via mask.	Selected COPD/respiratory failure; avoid with vomiting, severe agitation or inability to protect airway.

4. Setting priorities: oxygenation versus ventilation

Oxygenation: adjust FiO2 and PEEP, treat alveolar collapse/fluid/infection and reassess SpO2/ABG.
Ventilation: adjust rate, tidal volume and pressure support according to PaCO2/pH, obstructive disease and patient effort.
Synchrony: optimise trigger sensitivity, flow, inspiratory time and sedation/analgesia so the patient and machine work together.
Safety: limit excessive pressures, avoid over-oxygenation, monitor blood pressure and prevent ventilator-associated complications.

Lung-protective principle: Use the lowest effective tidal volume and airway pressure, allow adequate exhalation and accept a clinically appropriate CO2 level when necessary rather than causing volutrauma/barotrauma through aggressive ventilation.

5. Non-invasive ventilation (NIV)

Potential benefit	Candidate features	Contraindications or failure signs
CPAP	Conscious patient with cardiogenic pulmonary oedema or hypoxaemia who can protect the airway.	Vomiting, shock, reduced consciousness, severe agitation, facial trauma or inability to cooperate.
BiPAP/NIV	Hypercapnic COPD exacerbation, increased work of breathing and cooperative patient.	Worsening acidosis, exhaustion, persistent hypoxia, copious secretions or haemodynamic instability.
Mask safety	Correct size, leak management, pressure relief and frequent skin checks.	Large leak, pressure sores, panic, aspiration or delayed intubation.

NIV must be started where trained staff can monitor continuously and intubate if it fails. Explain the mask, sit the patient upright, allow them to hold it initially where possible and reassess work of breathing, mental state, gas exchange and haemodynamics within minutes—not hours.

6. Monitoring the ventilated patient

Monitor	What it tells you	Limitations
Clinical examination	Chest rise, breath sounds, synchrony, secretions, distress, skin colour and perfusion.	Can miss silent deterioration; repeat after movement and interventions.
SpO2	Oxygenation trend.	Delayed/false readings with poor perfusion, motion, nail products or carbon monoxide.
ETCO2 waveform	Ventilation, tube confirmation, perfusion and sudden changes.	Interpret with circulation, pulmonary disease and equipment status.
ABG/VBG	pH, PaCO2, PaO2, bicarbonate, lactate and metabolic status.	Snapshot only; correlate with trends and the clinical picture.
Pressures/volumes	Compliance, resistance, air trapping, leaks and delivered VT.	Machine values can mislead when tubing, filters or patient effort change.
Haemodynamics	PEEP/positive pressure effects on venous return and shock.	Blood pressure must be assessed with perfusion and urine output.

7. Ventilator alarms: a systematic response

DOPE for sudden deterioration: Displacement of tube, Obstruction of tube/circuit, Pneumothorax or pulmonary problem, Equipment failure. Assess the patient first; manually ventilate if in doubt.

Alarm	Common causes	Immediate actions
High pressure	Biting, kink, secretions, bronchospasm, reduced compliance, pneumothorax, water in tubing.	Assess patient, disconnect and BVM with oxygen if unstable, inspect tubing, suction, check chest and escalate.
Low pressure/low volume	Disconnection, cuff leak, tube displacement, circuit leak or inadequate effort.	Check connections/cuff/tube depth, ventilate manually and confirm capnography.
Apnoea	No patient trigger, sedation/neuromuscular weakness, disconnection or sensor problem.	Assess consciousness/breathing, ensure backup ventilation and call the airway team.
High minute volume	Pain, anxiety, fever, acidosis, hypoxia, sepsis or ventilator dyssynchrony.	Assess cause and synchrony; do not simply suppress respiratory drive without evaluation.
Low oxygen supply	Empty cylinder, pipeline disconnection, concentrator failure.	Switch to backup oxygen, check pressure and inform the receiving team.
Power/battery	Unplugged device, depleted battery, electrical failure.	Connect power and manually ventilate during transfer or malfunction.

8. Common complications of mechanical ventilation

Ventilator-associated pneumonia: hand hygiene, head elevation where appropriate, oral care, suctioning, circuit care and early liberation when safe.
Barotrauma/volutrauma: pneumothorax, subcutaneous emphysema and high pressures; investigate sudden desaturation or hypotension.
Hypotension: positive pressure reduces venous return; consider hypovolaemia, excessive PEEP, tension pneumothorax or myocardial dysfunction.
Auto-PEEP/dynamic hyperinflation: incomplete exhalation in asthma/COPD causes rising pressures, hypotension and worsening distress; allow longer expiratory time and seek expert review.
Oxygen toxicity/absorption atelectasis: titrate FiO2 to the target and treat underlying lung disease.
Pressure injuries: inspect lips, nares, ears, cheeks and skin under masks/tapes every shift and after movement.
Delirium, weakness and deconditioning: orientate, mobilise early when safe, manage pain, avoid unnecessary deep sedation and involve the ICU team.

9. Patient–ventilator synchrony

Dyssynchrony occurs when the ventilator’s timing or flow does not meet the patient’s demand. Clues include grimacing, accessory muscle use, double triggering, missed breaths, high peak pressure, tachycardia or agitation. Check pain, hypoxia, acidosis, fever, secretions, tube position, trigger sensitivity and mode before increasing sedation. Paralysis masks distress and should be used only for a clear indication with adequate analgesia/sedation.

10. Sedation, analgesia and neuromuscular blockade

Principle	Why it matters
Analgesia first	Pain from tube, suction, fractures or procedures can look like agitation and increase oxygen demand.
Lightest effective sedation	Allows neurological assessment, synchrony and earlier weaning while reducing delirium and hypotension.
Daily review	Check indication, target sedation score, interruptions, delirium, pain and readiness to reduce support.
Paralysis is not sedation	A paralysed patient can be awake and terrified; provide analgesia/sedation and eye/skin care.
Safety monitoring	BP, ECG, respiratory status, temperature, glucose, urine output and medicine interactions.

11. Transporting a ventilated patient

Confirm indication, airway depth/fixation, cuff status, mode/settings, alarms, oxygen reserve and battery life.
Bring a self-inflating bag with reservoir, backup oxygen, suction, spare tubes/SGA, capnography and emergency medicines.
Secure all tubing to prevent traction; position the patient with head/neck supported and pressure points protected.
Use continuous SpO2, ECG, BP and ETCO2 monitoring; assign a clinician to the airway, not just the monitor.
Before moving, pre-oxygenate if indicated and explain the plan; after every transfer check chest rise, tube depth, capnography and pressures.
Communicate ventilator settings, recent ABG, secretions, sedation, events and emergency contact pathway to the receiving team.

12. Emergency disconnection or ventilator failure

Patient first: If a ventilated patient becomes hypoxic, hypotensive or unresponsive, disconnect from the ventilator and manually ventilate with a self-inflating bag and oxygen while another team member troubleshoots. If manual ventilation is easy and the patient improves, suspect equipment/tube problems; if difficult, suspect obstruction, bronchospasm or pneumothorax.

Check oxygen source, power, circuit, filters, water traps and alarm limits.
Inspect tube depth, cuff, secretions and bite; suction only when indicated.
Listen for unilateral breath sounds, assess tracheal position and look for tension pneumothorax.
Call the airway/critical-care clinician early; do not silence alarms without finding the cause.

13. Weaning and liberation

Weaning begins when the cause of respiratory failure improves and the patient can maintain airway protection, adequate oxygenation and ventilation with reduced support. The ICU team considers mental state, cough, secretions, haemodynamics, gas exchange, respiratory muscle strength and a spontaneous breathing trial. Extubation requires a plan for reintubation and post-extubation support.

Readiness feature	Questions
Cause improved	Has pneumonia, shock, overdose, trauma or surgery stabilised?
Oxygenation	Can target oxygenation be maintained on low/moderate FiO2 and PEEP?
Ventilation	Is pH/PaCO2 acceptable with manageable work of breathing?
Neurological state	Can the patient wake, follow commands, cough and protect the airway?
Haemodynamics	Is blood pressure stable without escalating vasopressor support?
Secretions	Can the patient clear secretions and maintain airway hygiene?

14. Clinical scenarios

Scenario 1 — High-pressure alarm: A ventilated COPD patient suddenly alarms high pressure and becomes hypotensive. Assess the patient, disconnect and BVM with oxygen, check for kink/secretions/bronchospasm, allow exhalation and urgently exclude tension pneumothorax and auto-PEEP.

Scenario 2 — Low-volume alarm: After ambulance transfer, the low-volume alarm sounds and the waveform disappears. Manually ventilate, check connections and tube depth, assess cuff/circuit leak and confirm placement with capnography.

Scenario 3 — NIV failure: A patient on BiPAP is increasingly drowsy, vomiting and has falling SpO2. Remove the mask, suction/protect the airway, ventilate with BVM and call the advanced airway team; do not persist with NIV.

Scenario 4 — Sudden hypotension after PEEP increase: A septic patient becomes hypotensive after a pressure change. Reassess preload, right-heart function, pneumothorax, bleeding and sedation; involve the clinician rather than independently returning to arbitrary settings.

Scenario 5 — Transport disconnect: During movement, ETCO2 falls to zero. Stop, BVM with oxygen, check the tube/circuit, reconnect only after confirming function and reassess chest rise, SpO2 and waveform.

15. Ventilator handover checklist

Indication for ventilation, diagnosis, airway type/size/depth, cuff status and last confirmation.
Mode, FiO2, VT or pressure, rate, PEEP, pressure support, alarms and recent changes.
Latest SpO2/ETCO2/ABG, respiratory examination, secretions and suction frequency.
Analgesia, sedation, neuromuscular blockade, infusions, allergies and haemodynamic support.
Events during transfer, alarm causes, circuit changes, complications and response.
Plan for repeat gases, imaging, weaning, extubation or escalation.

16. Revision questions

What is the difference between oxygenation failure and ventilation failure?
Why can PEEP improve oxygenation but lower blood pressure?
What does the DOPE mnemonic stand for?
How do high-pressure and low-pressure alarms differ?
When is NIV unsafe or failing?
Why is paralysis not the same as sedation?
What must be carried during transport of an intubated patient?
What findings suggest auto-PEEP in asthma/COPD?
What are the main components of weaning readiness?
Why should an unstable ventilated patient be manually ventilated while troubleshooting?

17. Key take-home points

Mechanical ventilation supports oxygenation, ventilation and airway protection; it does not treat the underlying cause by itself.
Assess the patient before the machine, then use DOPE to troubleshoot sudden deterioration.
Protect the lung with appropriate volumes, pressures, PEEP, oxygen targets and adequate exhalation.
Monitor the full picture: chest movement, SpO2, ETCO2, ABG, pressures, haemodynamics and mental state.
Every transport needs a backup BVM, oxygen, suction, monitoring and a clear airway plan.

Selected authoritative resources

For EMT practice: Know the machine, but always treat the patient. When the ventilator alarms, call for help, maintain manual oxygenation and find the cause before changing settings.

Mechanical Ventilation: Modes, Settings, Alarms and EMT Safety Read More »

Advanced Life Support (ALS): Cardiac Arrest, Defibrillation and Post-ROSC Care

Why this matters: Advanced life support is a coordinated response to cardiac arrest and peri-arrest deterioration. The EMT must recognise arrest early, start high-quality CPR, use an AED/defibrillator safely, obtain vascular access when trained, identify reversible causes, support airway/ventilation and deliver a structured handover after return of spontaneous circulation (ROSC).

Safety and scope: Follow current AHA/ERC guidance, the Uganda Clinical Guidelines, equipment-specific instructions and your authorised scope. Drug concentrations, shock energies and pacing settings vary by system. ALS is team care: call for help early, assign roles and never allow a medication or airway task to delay compressions and defibrillation.

Learning outcomes

Recognise cardiac arrest and distinguish shockable from non-shockable rhythms.
Deliver effective CPR, defibrillation and ventilation with minimal interruptions.
Use a team-based ALS cycle, identify reversible Hs and Ts, and administer protocol-led medicines.
Recognise peri-arrest bradycardia and tachyarrhythmia requiring pacing, cardioversion or specialist escalation.
Provide structured post-ROSC care, including oxygenation, blood pressure, ECG, temperature and neurological protection.
Document timing, rhythm, shocks, medicines, airway, ETCO2 and response for clinical governance.

1. Recognising cardiac arrest

Ensure scene safety and use PPE.
Check responsiveness and normal breathing. Occasional gasps are agonal, not effective breathing.
Call for the resuscitation team/AED and check a central pulse only if trained; do not delay CPR for prolonged pulse searching.
Start compressions immediately when there is no normal breathing and no definite pulse.
Attach defibrillator/AED pads as soon as available while CPR continues.

Cardiac-arrest clock: Every minute without CPR and defibrillation lowers survival. Start compressions, attach pads, analyse rhythm and shock when indicated—then resume CPR immediately.

2. High-quality CPR

Element	Adult target/principle	Common error
Rate	100–120 compressions per minute.	Too slow, too fast or irregular.
Depth	At least 5 cm but avoid excessive depth; allow full recoil.	Shallow compressions or leaning on the chest.
Location	Centre of the chest/lower half of sternum on a firm surface.	Hands too high, too low or over the xiphisternum.
Interruptions	Keep pauses as short as possible, ideally under 10 seconds for rhythm checks/shock.	Long pauses for intubation, pulse checks or drug preparation.
Ventilation	Without advanced airway: 30 compressions to 2 breaths. With advanced airway: continuous compressions and one breath about every 6 seconds when protocolled.	Hyperventilation, excessive volume or failure to ventilate.
Switch compressor	Every about 2 minutes or sooner if fatigue, without pausing compressions.	Quality falls while the team hesitates to rotate.

3. Team roles and closed-loop communication

Team leader: overall plan, rhythm interpretation, reversible causes and decisions.
Compressor: high-quality compressions; announces fatigue and switches smoothly.
Airway/ventilation: mask seal, oxygen, adjunct/advanced airway, ventilation and capnography.
Defibrillator operator: pads, rhythm analysis, charging, safety checks and shock delivery.
Medication/access: IV/IO access, preparation, timing and flushes according to protocol.
Recorder: times compressions, rhythm checks, shocks, medicines, ETCO2, ROSC and handover.

Closed loop: The leader gives a named task; the receiver repeats it; the receiver reports completion and result. This prevents unrecognised missed adrenaline, unsafe shocks and duplicate doses.

4. Defibrillation and rhythm categories

Rhythm	Meaning	Immediate action
VF / pulseless VT	Chaotic or rapid ventricular electrical activity with no effective pulse.	Shock as soon as safely possible, then immediate CPR for about 2 minutes before re-analysis.
Asystole	No meaningful ventricular electrical activity.	CPR, adrenaline as protocolled, search reversible causes; do not shock asystole.
PEA	Organised electrical activity without a palpable pulse.	CPR, adrenaline and aggressive search for Hs and Ts; treat the cause.

5. Shockable rhythm cycle: VF/pulseless VT

Continue CPR while pads are attached; ensure everyone is clear before analysis and shock.
Deliver the manufacturer/protocol-recommended biphasic shock. Keep oxygen sources away from the chest and announce “all clear.”
Immediately resume CPR for about two minutes—do not pause to check a pulse unless there are signs of ROSC.
Obtain IV/IO access, give protocol-led adrenaline/epinephrine after the appropriate shock cycle and repeat at the recommended interval.
For persistent VF/pVT after further shocks, consider an antiarrhythmic such as amiodarone or lidocaine according to local ALS protocol.
Search for reversible causes throughout: hypoxia, hypovolaemia, electrolytes, hypothermia, tension pneumothorax, tamponade, toxins, thrombosis and trauma.

6. Non-shockable rhythm cycle: PEA/asystole

Start/continue CPR and confirm the rhythm in more than one lead or pad position when possible.
Give adrenaline/epinephrine as soon as IV/IO access is available according to protocol, then repeat at the authorised interval.
Do not waste time attempting defibrillation for true asystole.
Use capnography, ultrasound where available and clinical signs to assess CPR quality and reversible causes.
Reanalyse rhythm every about two minutes; if it becomes shockable, switch immediately to the shockable pathway.

7. Defibrillator safety

Dry the chest, remove medication patches and place pads with adequate separation; avoid placing directly over an implanted device.
Ensure no one is touching the patient, bed, oxygen tubing or stretcher during analysis and shock.
Keep hands and oxygen away from the shock field; follow the device’s charging and shock-confirmation sequence.
Resume compressions immediately after the shock and minimise pauses for rhythm checks.
Record energy, shock number, rhythm and response; a failed shock may reflect pad contact, severe hypoxia, acidosis, low energy or a non-shockable rhythm.

8. Advanced airway and ventilation in ALS

Start with effective BVM ventilation and an airway adjunct. An SGA or endotracheal tube may be considered by a competent provider without interrupting compressions for more than a brief interval. Continuous waveform capnography is used to confirm and monitor tube placement and CPR quality. Once an advanced airway is in place, avoid excessive ventilation: continuous compressions and slow, regular breaths according to the current protocol.

Sign	Meaning during CPR	Action
Sudden ETCO2 rise	Possible ROSC, improved circulation or change in compression quality.	Check pulse and rhythm without prolonging a pause; continue post-ROSC care if circulation returned.
Low/falling ETCO2	Poor compressions, inadequate perfusion, hyperventilation, disconnection or prolonged arrest.	Improve compression quality, check circuit/airway, avoid hyperventilation and reassess causes.
Absent waveform	Dislodged tube, oesophageal placement, disconnection, apnoea or very low flow.	Ventilate by BVM, inspect equipment and confirm placement immediately.

9. Vascular access and ALS medicines

Medicine/intervention	Role	Safety and monitoring
Adrenaline/epinephrine	Improves coronary/cerebral perfusion pressure during arrest; used on the shockable or non-shockable pathway at protocolled intervals.	Use the correct concentration and route. Record every dose/time; do not give repeated unrecorded doses.
Amiodarone or lidocaine	Considered for refractory VF/pVT after shocks according to local algorithm.	Monitor rhythm, blood pressure and cumulative dose; correct hypoxia/electrolytes.
Magnesium	Selected torsades de pointes or specific electrolyte-related arrhythmia.	Not routine for every arrest; monitor renal function and rhythm.
Calcium/bicarbonate	Only for specific indications such as hyperkalaemia, calcium-channel blocker toxicity or severe sodium-channel blockade.	Routine use in undifferentiated arrest is not recommended; obtain senior/toxicology guidance.
IV/IO access	Allows rapid medicine/fluid delivery when IV is difficult.	Secure line, flush according to protocol and document site/complications.

10. Reversible causes: Hs and Ts

Cause	Clues	Targeted action
Hypoxia	Low SpO2 before arrest, airway obstruction, chest disease, absent ventilation.	Open/suction airway, oxygenate, ventilate, confirm device and treat the cause.
Hypovolaemia	Bleeding, dehydration, burns, weak pulse, flat veins, trauma.	Control bleeding, IV/IO access, warmed crystalloid/blood protocol and rapid source control.
Hydrogen ion (acidosis)	Prolonged arrest, renal failure, shock, DKA or toxin exposure.	High-quality CPR/ventilation and treat cause; bicarbonate only for specific indications.
Hypo-/hyperkalaemia/metabolic	Weakness, renal disease, dialysis, ECG changes, medication exposure.	Point-of-care/lab testing and protocol-led calcium, insulin/glucose, bicarbonate or other therapy.
Hypothermia/hyperthermia	Abnormal core temperature, environmental exposure, drug toxicity, sepsis.	Measure core temperature and use controlled rewarming/cooling.
Tension pneumothorax	Sudden unilateral absent breath sounds, distended neck veins, shock, high airway pressure.	Immediate decompression by trained provider; do not wait for imaging in arrest.
Tamponade	Trauma, muffled heart sounds, raised venous pressure, PEA, narrow pulse pressure.	Urgent ultrasound/surgical or pericardial intervention by specialists.
Toxins	Packets, pupils, unusual ECG, seizures, exposure history or multiple victims.	PPE, decontamination, poison-centre advice and toxin-specific antidotes.
Thrombosis—pulmonary	Sudden collapse, hypoxia, risk factors, PEA, signs of DVT.	Consider thrombolysis or embolectomy pathway with senior team.
Thrombosis—coronary	Ischaemic symptoms, ST elevation, ventricular arrhythmia.	Post-ROSC ECG and urgent reperfusion pathway.
Trauma	External/internal bleeding, chest injury, head injury.	Haemorrhage control, airway/ventilation, pelvic/limb stabilisation and trauma-centre transfer.

11. Peri-arrest bradycardia

Bradycardia matters when it causes hypotension, altered mental state, shock, ischaemic chest discomfort or acute heart failure. First correct hypoxia, review medicines and look for myocardial infarction, electrolyte problems or conduction disease.

Assess airway/breathing/circulation, attach ECG/BP/SpO2 and obtain IV/IO access.
Give atropine or other first-line treatment only according to local protocol and contraindications.
If unstable or unresponsive to initial therapy, prepare transcutaneous pacing and/or infusion support by an authorised clinician.
Provide analgesia/sedation for pacing when safe, but never delay lifesaving electrical support.
Escalate early for transvenous pacing or specialist care.

12. Peri-arrest tachyarrhythmia

Pattern	Assessment	Immediate direction
Unstable tachycardia with pulse	Shock, hypotension, altered mental state, ischaemic chest pain or acute heart failure.	Synchronised cardioversion by trained clinician; sedate if feasible without delaying shock.
Stable narrow-complex regular tachycardia	Regular rhythm, often sudden onset; check ECG and cause.	Vagal manoeuvres/adenosine only by protocol and monitoring; seek senior review.
Stable atrial fibrillation/flutter	Irregular or saw-tooth rhythm; assess duration, anticoagulation and cause.	Rate/rhythm strategy and anticoagulation decisions are clinician-led.
Wide-complex tachycardia	Assume VT until proven otherwise, especially with structural heart disease.	Urgent expert review; avoid inappropriate AV-nodal blockade in pre-excited AF.

13. ROSC recognition

Sudden organised rhythm with a palpable central pulse.
Abrupt rise in ETCO2, spontaneous breathing, purposeful movement or improved skin perfusion.
Do not stop compressions solely because the monitor shows an organised rhythm; check a pulse and signs during a brief pause.

14. Immediate post-ROSC care

Airway: maintain patency; use an advanced airway only when it can be confirmed and monitored without compromising oxygenation.
Breathing: titrate oxygen to the prescribed target, avoid both hypoxaemia and unnecessary hyperoxia, and use capnography/ABG where available.
Circulation: continuous ECG/BP, IV/IO access, fluids/vasopressors as directed and treatment of shock.
12-lead ECG: identify STEMI or other cause and activate the reperfusion pathway.
Disability: glucose, pupil/neurological assessment, seizure recognition and sedation/analgesia review.
Temperature and brain protection: prevent fever, manage seizures and follow the receiving critical-care protocol.
Cause and destination: identify the reason for arrest, communicate resuscitation details and transfer to a capable hospital.

15. ALS after cardiac arrest in special circumstances

Situation	Key modification
Pregnancy	Call obstetric/neonatal help, optimise left uterine displacement, early airway support and follow maternal arrest protocol.
Trauma	Control catastrophic bleeding, address airway/chest injury and consider resuscitative thoracostomy or surgery by trained teams.
Drowning	Ventilation is especially important; remove from water safely, manage hypothermia and consider cervical injury by mechanism.
Hyperkalaemia	Look for renal failure/dialysis and peaked T waves/wide QRS; give calcium and shifting therapy only per protocol.
Opioid/toxin arrest	PPE, airway/ventilation, antidote when indicated and protect rescuers from contamination.
Hypothermia	Measure core temperature, handle gently, rewarm while continuing resuscitation and use local temperature-specific algorithm.

16. Clinical scenarios

Scenario 1 — Witnessed VF: A patient collapses in a clinic, has agonal gasps and VF on the monitor. Start CPR, charge and shock safely, resume compressions immediately, establish IV/IO access, give protocol-led medicines and reassess every cycle while searching reversible causes.

Scenario 2 — PEA after trauma: A motorcyclist is pulseless with organised electrical activity, distended neck veins and absent left breath sounds. Continue CPR, ventilate, call for immediate chest decompression by the trained provider and control haemorrhage—do not waste time shocking PEA.

Scenario 3 — ROSC in the ambulance: ETCO2 rises suddenly and a pulse returns. Stop compressions briefly to confirm, secure the airway, titrate oxygen, support blood pressure, obtain ECG/glucose, prevent fever and give a complete handover.

Scenario 4 — Bradycardic collapse: An inferior-MI patient has HR 30, hypotension and confusion. Oxygenate, monitor, obtain access, follow the bradycardia algorithm and prepare pacing while the senior clinician treats the cause.

Scenario 5 — Refractory VF: VF persists after shocks and adrenaline. Check pad contact, compression quality, oxygenation, electrolytes, toxins and coronary thrombosis; give an antiarrhythmic only through the authorised protocol and continue high-quality CPR.

17. Resuscitation documentation

Collapse/witnessed status, bystander CPR, first rhythm and time CPR started.
Every rhythm check and shock: time, rhythm, energy/device and response.
Compression quality, pauses, compressor changes, airway devices, ventilation and capnography.
IV/IO sites, medicines/concentrations/doses/times, fluids and adverse effects.
Reversible causes considered/treated and consultations made.
ROSC time, vital signs, ECG, glucose, neurological status, airway confirmation and destination.

18. Revision questions

What are the differences between VF/pVT and PEA/asystole management?
Why must compressions resume immediately after a shock?
List the Hs and Ts and give one bedside clue for each.
What does a sudden ETCO2 rise suggest during CPR?
Why is routine calcium or bicarbonate not given in every arrest?
What findings make a tachyarrhythmia “unstable”?
What are the first post-ROSC priorities?
Why is closed-loop communication important in ALS?
When should a rescue airway be used instead of repeated intubation attempts?
Which details must appear in a resuscitation record?

19. Key take-home points

High-quality CPR and early defibrillation are the foundations of ALS.
Shock VF/pVT; do not shock true asystole or PEA.
Use waveform capnography to confirm airway placement, monitor CPR and recognise possible ROSC.
Search for and treat reversible causes throughout every arrest cycle.
After ROSC, protect oxygenation, ventilation, blood pressure, temperature and the brain while treating the cause.
A disciplined team, accurate timing and clear handover are clinical interventions, not paperwork.

Selected authoritative resources

For EMT practice: Start early, compress well, shock safely, ventilate effectively, think Hs and Ts, and treat ROSC as the beginning of critical care—not the end of resuscitation.

Advanced Life Support (ALS): Cardiac Arrest, Defibrillation and Post-ROSC Care Read More »

Emergency Airway Management: Assessment, Devices, Ventilation and Safety

Why this matters: Airway failure kills within minutes, yet many emergencies can be prevented by early recognition, positioning, suction, oxygenation and effective bag-mask ventilation. EMT students must know what they can do independently, what requires an advanced provider and how to maintain oxygen delivery during transport and handover.

Scope and safety: Follow your training level, Uganda Clinical Guidelines, local ambulance protocols and medical direction. Intubation and advanced airway procedures should be attempted only by trained, competent providers with a high success rate, backup plans and continuous waveform capnography. Never allow a device attempt to interrupt high-quality CPR or delay basic oxygenation.

Learning outcomes

Recognise threatened, obstructed and failed airways using a structured primary survey.
Perform positioning, manual opening, suction, basic adjuncts and bag-mask ventilation safely.
Select an oropharyngeal, nasopharyngeal or supraglottic device when trained and identify contraindications.
Prepare for advanced airway intervention, failed-airway rescue and post-intubation care without losing oxygenation.
Use pulse oximetry, capnography, chest movement and clinical signs to confirm and monitor ventilation.
Document airway findings, interventions, attempts, confirmation and patient response.

1. Airway anatomy and physiology for EMTs

The upper airway conducts air from the nose and mouth to the larynx. The tongue, soft palate, blood, vomit, swelling, foreign bodies and facial trauma can obstruct it. The larynx protects the trachea during swallowing; the epiglottis and vocal cords are dynamic structures that may swell or spasm. Oxygenation depends on alveolar ventilation, perfusion and inspired oxygen, while ventilation means removal of carbon dioxide. A patient can have acceptable SpO2 briefly while ventilation and CO2 are worsening.

Problem	Mechanism	Clues
Loss of tone	Reduced consciousness allows tongue/soft palate to fall backward.	Snoring, paradoxical chest movement, absent response to voice.
Secretions/vomit/blood	Fluid blocks the oropharynx or is aspirated.	Gurgling, bubbling, coughing, cyanosis and falling SpO2.
Swelling	Anaphylaxis, burns, infection or trauma narrows the airway.	Hoarseness, stridor, drooling, dysphagia, tongue/lip oedema.
Bronchospasm	Lower airway smooth muscle narrows bronchi.	Wheeze, prolonged expiration, increased work of breathing or silent chest.
Foreign body	Food, teeth, blood clot or object occludes airflow.	Sudden cough/stridor, inability to speak, unilateral air entry change.
Ventilatory failure	Fatigue, neuromuscular weakness, CNS depression or chest injury prevents adequate breaths.	Slow/irregular breathing, poor chest rise, rising ETCO2, exhaustion or altered consciousness.

2. Primary airway assessment

Scene and PPE: identify trauma, fire/smoke, chemicals, water, blood and violence. Protect yourself before contact.
Responsiveness: speak, touch and assess response. A patient who can speak clearly has a patent airway at that moment, but may still deteriorate.
Look: chest rise, work of breathing, cyanosis, accessory muscle use, facial burns, blood, vomit, swelling and position.
Listen: snoring, gurgling, stridor, wheeze, silence, hoarse voice and abnormal breath sounds.
Feel: airflow at mouth/nose, tracheal position, facial/neck swelling, subcutaneous emphysema and chest movement.
Check breathing quality: rate, depth, regularity, fatigue, SpO2 and, when available, ETCO2. Agonal gasps are not normal breathing.
Anticipate difficulty: obesity, pregnancy, cervical injury, facial trauma, burns, blood/vomit, limited mouth opening, beard, dentures, paediatric anatomy and previous difficult airway.

“LOOK–LISTEN–FEEL–ACT”: Look for obstruction and chest rise; listen for snoring/gurgling/stridor; feel for air movement; then act with positioning, suction, adjuncts and ventilation.

3. Positioning and manual airway opening

Situation	Position/technique	Reason and caution
No trauma suspected	Head-tilt/chin-lift; align ear with sternal notch where possible.	Lifts the tongue from the posterior pharynx and improves patency.
Possible cervical spine injury	Jaw thrust with manual in-line stabilisation; avoid unnecessary neck movement.	Maintains airway while reducing spinal motion; airway and oxygenation still take priority.
Conscious breathless patient	Allow position of comfort, usually sitting forward.	Reduces work of breathing; do not force supine positioning.
Unconscious but breathing	Recovery position if no contraindication and while monitoring spine/trauma.	Allows drainage and reduces aspiration; reassess frequently.
Pregnancy or obesity	Ramped/shoulder elevation and left uterine displacement where appropriate.	Improves airway alignment and oxygen reserve; get extra help early.

4. Suction and clearing the airway

Use a rigid Yankauer for visible vomit, blood or secretions in the mouth and a soft catheter for deeper gentle suction when trained.
Pre-oxygenate where possible; suction under direct vision, avoiding blind sweeping that can push a foreign body deeper.
Limit each suction attempt to the local protocol, commonly no more than 10–15 seconds in an adult, with re-oxygenation between attempts.
Monitor heart rate, SpO2 and patient response; vigorous suction can trigger hypoxia, bradycardia, laryngospasm or trauma.
Prepare a backup suction source and battery; a blocked catheter or full canister can create a false sense of readiness.

5. Basic airway adjuncts

Adjunct	Indication	Contraindication/risks	Practical check
Oropharyngeal airway (OPA)	Unconscious patient without a gag reflex who needs airway support.	Conscious or semi-conscious patient with gag/cough; can cause vomiting, laryngospasm or trauma.	Choose correct size (mouth corner to angle of jaw), insert with appropriate technique and reassess patency.
Nasopharyngeal airway (NPA)	Reduced consciousness with an intact gag reflex or trismus; supports the nasal passage.	Suspected basilar skull fracture, severe nasal trauma or obstruction; epistaxis risk.	Measure nostril to tragus/angle of jaw, lubricate, insert gently, never force against resistance.
Supraglottic airway (SGA)	Rescue airway for apnoea or inadequate ventilation when trained and authorised.	Intact gag, caustic ingestion, severe airway obstruction below the device, limited mouth opening or local contraindication.	Confirm chest rise, bilateral breath sounds where feasible, waveform capnography and absence of significant leak.

Never use an adjunct as a substitute for observation. A correctly placed OPA/NPA can become obstructed by secretions, displaced by movement or inadequate when swelling progresses. Reassess after every transfer, suction and position change.

6. Bag-mask ventilation (BVM)

BVM is the most important rescue skill when a patient is apnoeic or breathing inadequately. Use a two-person technique whenever possible: one provider maintains a two-handed mask seal and jaw position while the second squeezes the bag and watches the chest.

Choose an appropriate mask that covers the bridge of the nose, mouth and chin without covering the eyes.
Position the head, open the airway and suction visible secretions. Use an adjunct when indicated.
Use the “EC” hand position: thumb and index finger form a C around the mask while the remaining fingers lift the mandible (E).
Deliver the smallest volume that produces visible chest rise; avoid forceful or rapid squeezing.
Use oxygen and a reservoir when available; monitor chest rise, SpO2, pulse and ETCO2.
If the chest does not rise, reposition, reseal, suction, check the valve/tubing, insert an adjunct and consider obstruction or pneumothorax.
Continue reassessment; excessive ventilation increases gastric inflation, regurgitation, aspiration and intrathoracic pressure.

BVM troubleshooting

Problem	Likely causes	Correction
No chest rise	Poor seal, blocked airway, wrong position, closed valve, severe bronchospasm.	Reposition, two-person seal, suction, adjunct, inspect equipment, escalate to advanced airway.
Stomach inflation	Excessive pressure/volume, rapid ventilation, oesophageal insufflation.	Slow smaller breaths, improve airway alignment and consider SGA/intubation by trained provider.
Falling SpO2 despite ventilation	Disconnection, inadequate oxygen source, pneumothorax, pulmonary oedema, severe shunt or wrong placement.	Check equipment and tube/SGA, auscultate, use waveform capnography and seek advanced support.
Sudden resistance	Bite, kink, obstruction, bronchospasm or equipment blockage.	Look inside the mouth, change position/adjunct, suction and treat bronchospasm per protocol.

7. Oxygen therapy and monitoring

Oxygen is a medicine: give it when there is hypoxaemia, respiratory distress, shock, cardiac arrest or another protocol indication, then titrate to the target range. Avoid both untreated hypoxia and unnecessary prolonged hyperoxia. Pulse oximetry is useful but can be inaccurate with motion, poor perfusion, nail products, carbon monoxide exposure or severe anaemia.

Device	Typical use	Safety points
Nasal cannula	Low-flow support for a spontaneously breathing patient with mild hypoxaemia.	Check nares, comfort, flow and actual SpO2 response.
Simple face mask	Moderate oxygen requirement.	Never run at very low flow because rebreathing CO2 can occur.
Non-rebreather mask	High inspired oxygen for severe hypoxaemia while preparing definitive care.	Keep reservoir inflated; it does not provide ventilation to an apnoeic patient.
Bag-mask with reservoir	Apnoea, agonal breathing or inadequate ventilation.	Requires seal, airway opening and controlled breaths; monitor for gastric inflation.
CPAP/NIV	Selected conscious patients with respiratory failure who can protect the airway and cooperate.	Not for vomiting, severe agitation, facial trauma or inability to protect the airway; monitor continuously.

8. Foreign-body airway obstruction

Mild obstruction: encourage effective coughing and observe closely; do not blindly sweep the mouth.
Severe obstruction in a conscious adult/child: call for help and use age-appropriate back blows and abdominal/chest thrusts according to current BLS training.
Becomes unresponsive: lower safely, begin CPR, look for a visible object before breaths and activate advanced help.
Infant: use infant-specific back slaps and chest thrusts; never abdominal thrusts.
After removal: evaluate for residual obstruction, aspiration, rib injury or delayed airway oedema; medical assessment is needed even if the object comes out.

9. Preparing for an advanced airway

Advanced airway placement is a team procedure, not a single person’s rescue attempt. The goal is oxygenation and ventilation with the fewest interruptions and highest first-pass success. Before the attempt, plan for the best device, backup SGA, suction, oxygenation method, waveform capnography, drugs/analgesia if authorised and a failed-airway pathway.

Preparation	Questions to answer
Patient	Why is the airway needed? Can the patient be oxygenated now? Is there aspiration, trauma, swelling, burns, cervical injury or difficult anatomy?
People	Who is the airway operator, assistant, monitor, drug nurse and team leader? Who will call for help?
Equipment	Suction working? BVM and oxygen? Laryngoscope/video device? Tube sizes? SGA? Bougie/stylet? Capnography? Tape/fixation? Backup surgical airway capability?
Plan A–D	Best attempt, optimisation, rescue oxygenation with SGA/BVM, and emergency front-of-neck access by trained experts.
Aftercare	Tube/SGA confirmation, fixation, ventilation plan, analgesia/sedation, gastric decompression if indicated and frequent reassessment.

10. Endotracheal intubation and confirmation

Only trained providers should intubate. A tube in the oesophagus or a displaced tube is immediately life-threatening. Continuous waveform capnography is the most reliable method to confirm and monitor tracheal placement in a perfusing patient, supplemented by chest rise, bilateral breath sounds, absence of gastric sounds, tube depth and clinical response. A single misting sign or initial SpO2 improvement is not enough.

Pre-oxygenate and maintain oxygen delivery between attempts; use apnoeic oxygenation or BVM as trained.
Limit attempts and time; stop early for falling SpO2, bradycardia, poor view or worsening physiology.
After placement, ventilate gently, apply waveform capnography, secure the tube and record depth at the teeth/lips.
Reconfirm after movement, ambulance loading, transfer, deterioration or a sudden change in ETCO2.
If capnography is absent, troubleshoot the circuit and tube immediately while ventilating by BVM and seeking help.

11. Capnography interpretation

ETCO2 pattern	Possible explanation	Action
Persistent flat line after intubation	Oesophageal intubation, disconnection, apnoea, very low pulmonary blood flow or faulty sensor.	Immediately ventilate with BVM, check connections and tube; remove/reposition if placement is not confirmed.
Sudden loss of waveform	Dislodged tube, disconnected circuit, blocked tube or cardiac arrest.	Assess patient and equipment together; begin rescue ventilation and CPR when indicated.
Low/decreasing ETCO2 during CPR	Poor compression quality, low perfusion, prolonged arrest or excessive ventilation.	Improve CPR quality, minimise pauses, check airway and consider reversible causes.
High ETCO2 with prolonged plateau	Hypoventilation, severe bronchospasm, rebreathing or increased CO2 production.	Check rate/volume, circuit, airway pressures and clinical causes; avoid simply hyperventilating.
Sudden rise with ROSC	Improved pulmonary blood flow after return of spontaneous circulation.	Reassess pulse, blood pressure, oxygenation and post-arrest care.

12. Rapid sequence induction (RSI) safety concepts

RSI combines pre-oxygenation, an induction agent and neuromuscular blockade to facilitate intubation. It is a high-risk procedure requiring an experienced airway clinician, a full plan for hypotension and a rescue airway. EMT students should understand the sequence, monitoring and complications even if they do not administer the drugs.

Prepare: monitors, IV/IO access, suction, oxygen, drugs, capnography, backup devices and post-intubation sedation.
Optimise: correct hypoxaemia, hypotension, acidosis and positioning where possible; use a ramped position in obesity/pregnancy.
Pre-oxygenate: maximise oxygen reserve; use BVM or NIV when indicated and safe.
Induce and paralyse: drug choice is clinician-led and patient-specific; anticipate hypotension, apnoea and difficult ventilation.
First-pass attempt: use the best operator/device; stop if oxygenation worsens.
Confirm and secure: waveform capnography, chest assessment, fixation, analgesia/sedation and ventilator/BVM plan.

13. Failed airway and “cannot oxygenate” response

Priority is oxygenation, not repeated laryngoscopy. If intubation fails, return to BVM with two-person seal, insert a supraglottic airway if trained, suction, optimise position and call the most experienced airway clinician. A surgical airway is a last-resort procedure for trained experts when oxygenation cannot be achieved.

Declare the failed attempt and communicate the next plan clearly.
Use a time/attempt limit and protect the patient from repeated trauma.
Maintain oxygenation between attempts; monitor SpO2, ECG, blood pressure and ETCO2.
Consider reversible causes: laryngospasm, bronchospasm, tension pneumothorax, equipment failure, oesophageal placement and severe hypovolaemia.
Document attempts and complications for future airway planning.

14. Special airway situations

Situation	Airway priorities
Trauma/cervical injury	Jaw thrust, manual in-line stabilisation, suction, oxygenation and early expert help. Airway takes priority over perfect spinal immobilisation.
Facial burns/inhalation injury	Look for soot, hoarseness, stridor, facial burns and enclosed-space exposure. Oedema can progress; prepare early advanced airway support.
Maxillofacial bleeding	Position to drain if safe, aggressive suction, two-person BVM and early surgical/anaesthetic help.
Paediatric airway	Large occiput, narrow airway and rapid desaturation; use age/size equipment, gentle ventilation and paediatric protocols.
Pregnancy	Reduced oxygen reserve and aspiration risk; ramp position, left uterine displacement, early help and avoid prolonged apnoea.
Obesity	Ramped position, larger equipment, effective pre-oxygenation and anticipation of difficult mask ventilation.
Neuromuscular weakness	Weak cough and fatigue may precede hypoxaemia; monitor ventilation/ETCO2 and involve critical care early.

15. Airway complications

Aspiration: suction, lateral/recovery positioning when appropriate, oxygen/ventilation and urgent assessment for pneumonitis or pneumonia.
Laryngospasm: remove stimulus, jaw thrust, positive-pressure oxygen and advanced management if persistent.
Bronchospasm: wheeze, high airway pressures and poor chest rise; bronchodilator and escalation according to protocol.
Tube displacement: sudden desaturation, absent waveform or unequal breath sounds; ventilate and confirm immediately.
Right mainstem intubation: unilateral breath sounds and rising pressures; check depth and reposition by the airway clinician.
Pneumothorax: sudden hypoxia, hypotension, unilateral silence and increased resistance; treat as a time-critical reversible cause.
Pressure injury and gastric inflation: avoid excessive ventilation pressure and volume; use a decompression plan when indicated.

16. Clinical scenarios

Scenario 1 — Snoring after overdose: A drowsy patient has slow breathing and loud snoring. Reposition, open the airway, suction if needed, insert an appropriate adjunct, assist ventilation and check glucose/oxygenation. Do not wait for complete apnoea.

Scenario 2 — Facial trauma: Blood and loose teeth fill the mouth after a road crash. Use PPE, suction under direct vision, jaw thrust/manual stabilisation, high-flow oxygen and two-person BVM; call an advanced airway team early.

Scenario 3 — Failed intubation: After one poor view the patient’s SpO2 falls. Stop repeated attempts, ventilate with a two-person mask technique, insert a rescue SGA if trained, use capnography and communicate the failed-airway plan.

Scenario 4 — Sudden ETCO2 loss in transit: A ventilated patient suddenly desaturates and the waveform disappears. Check the patient, tube, circuit, oxygen source and capnography sensor simultaneously; ventilate with BVM and treat dislodgement, obstruction, disconnection or arrest.

Scenario 5 — Burn inhalation: A patient rescued from a smoky room is initially talking but becomes hoarse with soot around the mouth. Monitor closely, give oxygen, prepare early airway support and transfer urgently because swelling can make later intubation impossible.

17. Airway equipment checklist

Category	Minimum readiness check
Oxygen/ventilation	Cylinder pressure, regulator, tubing, reservoir, BVM, masks, PEEP valve if used.
Suction	Power, tubing, canister, Yankauer, soft catheters and backup battery/manual suction.
Basic adjuncts	OPA/NPA range, lubricant, tape, bite block, forceps only if authorised.
Advanced airway	SGA sizes, laryngoscope/video device, blades, tubes, stylet/bougie, syringe, cuff manometer and securing material.
Monitoring	Pulse oximeter, ECG, non-invasive BP, waveform capnography and temperature where available.
Rescue	Backup BVM, spare oxygen, difficult-airway plan, emergency front-of-neck kit for trained teams and PPE.

18. Documentation and handover

Initial airway patency, voice, secretions, obstruction, breathing effort, SpO2/ETCO2 and neurological state.
Position, suction, oxygen device/flow, adjunct size, BVM technique and response.
Advanced airway device, operator, number of attempts, view, tube depth, confirmation method, ETCO2 waveform and fixation.
Ventilation settings or BVM rate/volume, airway pressures, sedation/analgesia and haemodynamic response.
Complications, reassessments after movement and exact handover time/person.

19. Revision questions

Why can a patient have a normal SpO2 while ventilation is failing?
When is an OPA unsafe, and what alternative adjunct may be considered?
List four causes of “no chest rise” during BVM ventilation.
Why is continuous waveform capnography important after intubation?
What is the priority after a failed intubation attempt with falling SpO2?
How does inhalation injury change the airway plan?
What signs suggest right mainstem intubation or tube displacement?
Why should ventilation use the smallest volume that produces visible chest rise?
What equipment must be checked before an advanced airway attempt?
What airway information belongs in a structured handover?

20. Key take-home points

Open, suction, oxygenate and ventilate before attempting advanced procedures.
Two-person BVM, good positioning and continuous reassessment save lives.
Airway devices are not self-monitoring—confirm chest rise, physiology and waveform capnography.
Limit attempts, maintain oxygenation and move early to a rescue plan.
Post-intubation care is an ongoing process: secure, sedate/analgesia as prescribed, ventilate, monitor and recheck after movement.

Selected authoritative resources

For EMT practice: The best airway is the one that delivers oxygen, protects the patient and can be confirmed continuously. Build a plan, keep a rescue option ready and never let a difficult procedure replace basic ventilation.

Emergency Airway Management: Assessment, Devices, Ventilation and Safety Read More »

Hypersensitivity Reactions and Emergency Antidotes: Recognition, Use and Safety

Why this matters for EMT students: Allergic and immune-mediated reactions can progress from an itchy rash to airway obstruction and distributive shock within minutes. Poisoning emergencies may look similar to allergy—wheeze, collapse, vomiting, altered consciousness or seizures—but require a different antidote and transport plan. The EMT’s value is early recognition, correct first actions, prevention of further exposure, repeated ABCDE assessment and precise handover.

Safety notice: This is an educational guide. Use the current Uganda Clinical Guidelines, local emergency drug concentrations, poison-centre advice and medical direction. Never delay airway, breathing and circulation support while searching for a named antidote. Antidotes are adjuncts; many patients need oxygen, ventilation, fluids, ECG monitoring, glucose correction, seizure control and critical care.

Learning outcomes

Differentiate allergy, intolerance, anaphylaxis, angioedema and non-immune hypersensitivity.
Explain the four Gell–Coombs hypersensitivity mechanisms and their clinical examples.
Recognise life-threatening airway, breathing and circulation features and start an anaphylaxis response promptly.
Identify severe cutaneous adverse reactions, serum sickness and drug-induced organ injury that need urgent referral.
Match common poisoning patterns with antidotes while understanding indications, limitations, interactions and monitoring.
Document exposures, timing, treatment and response so the receiving team can continue care safely.

1. Key terms

Term	Meaning and emergency relevance
Allergy	An immune-mediated reaction to an otherwise harmless antigen; symptoms can be mild, severe or delayed.
Hypersensitivity	An exaggerated or inappropriate immune response that causes tissue injury. It includes allergic and non-allergic mechanisms.
Intolerance	An unpleasant reaction that is not immune-mediated, such as nausea from an opioid or flushing from niacin.
Anaphylaxis	A rapid, potentially fatal systemic reaction with airway, breathing or circulation compromise, usually with skin/mucosal features but sometimes without them.
Angioedema	Deeper swelling of skin, lips, tongue, larynx or bowel. It may be histamine-mediated or bradykinin-mediated and can obstruct the airway.
Antidote	A medicine or intervention that prevents, binds, neutralises or reverses a specific toxin effect. It never replaces resuscitation and observation.

2. Gell–Coombs hypersensitivity types

Type	Mechanism	Examples	Time course
I — immediate	IgE activates mast cells and basophils; histamine, tryptase, leukotrienes and other mediators are released.	Anaphylaxis, allergic asthma, urticaria, food allergy, latex reaction.	Seconds to minutes; can be biphasic.
II — antibody-mediated cytotoxic	IgG/IgM bind cell or tissue antigens, activating complement or cellular destruction.	Haemolytic transfusion reaction, autoimmune haemolytic anaemia, some drug-induced cytopenias.	Hours to days.
III — immune-complex	Circulating antigen–antibody complexes deposit in tissues and activate complement.	Serum sickness, some vasculitides, post-infectious inflammation.	Days to weeks.
IV — delayed T-cell	Sensitised T cells release cytokines or directly injure cells; no antibody is required.	Contact dermatitis, tuberculin reaction, severe cutaneous drug reactions.	Usually 48–72 hours or longer.

Clinical caution: A previous mild reaction does not guarantee the next reaction will be mild. Conversely, a rash alone does not prove anaphylaxis. Grade the current airway, breathing and circulation every time.

3. Common triggers in Ugandan emergency practice

Medicines: beta-lactam antibiotics, sulfonamides, NSAIDs, anticonvulsants, opioids, anaesthetic agents, vaccines and biologics.
Foods: groundnuts, nuts, milk, eggs, fish, shellfish, fruits and hidden ingredients.
Venom and bites: bees, wasps, ants, snakes and other arthropods.
Latex and occupational exposures: gloves, catheters, tourniquets and equipment.
Contrast and blood products: immediate reactions, delayed rashes or haemolysis.
Non-immune mimics: radiocontrast reactions, exercise, heat, alcohol, opioids or direct mast-cell activation.

4. Recognising anaphylaxis

Think anaphylaxis when illness begins suddenly after a plausible exposure and there is airway, breathing or circulation compromise, usually with skin or mucosal change. Skin signs can be absent, especially in severe shock. Gastrointestinal symptoms may be prominent after food exposure.

System	Findings	Danger sign
Airway	Throat tightness, hoarse voice, tongue/lip swelling, stridor, drooling, difficulty swallowing.	Rapidly worsening voice, stridor, inability to speak or maintain secretions.
Breathing	Wheeze, cough, chest tightness, tachypnoea, hypoxia, cyanosis or silent chest.	Severe bronchospasm, exhaustion, falling SpO2 or respiratory arrest.
Circulation	Dizziness, collapse, tachycardia, hypotension, pallor, clammy skin, weak pulse.	Shock, altered consciousness or cardiac arrest.
Skin/mucosa	Flushing, itching, urticaria, erythema, angioedema.	Do not wait for a rash before treating airway/breathing/circulation compromise.
Gastrointestinal	Cramping, vomiting or diarrhoea, especially after food exposure.	Persistent vomiting with shock or airway swelling.

5. Emergency treatment of anaphylaxis

Call for help and stop the trigger: stop an infusion or remove a visible stinger if safe; do not delay treatment while looking for the trigger.
Position correctly: lay flat with legs raised if shock is present. Allow a breathless patient to sit with legs outstretched, but never allow a shocked patient to stand or walk. Place an unconscious breathing patient in the recovery position.
Give IM adrenaline/epinephrine immediately into the outer mid-thigh using the concentration and age/weight protocol available locally. Adrenaline is first-line for airway, breathing or circulation problems. Do not substitute an antihistamine or steroid.
Reassess after about five minutes: repeat IM adrenaline if airway, breathing or circulation problems persist, according to protocol. Record time and dose.
Support ABCDE: high-concentration oxygen when indicated, airway equipment and suction ready, IV/IO access by trained personnel, rapid crystalloid for persistent shock and continuous monitoring.
Treat bronchospasm or upper-airway obstruction: nebulised bronchodilator or nebulised adrenaline may be added by protocol; these never replace IM adrenaline. Prepare early for advanced airway management.
Transport and observe: all anaphylaxis patients require medical assessment because symptoms can recur after initial improvement. Observation time depends on severity, treatment and local guidance.

Adrenaline safety: Use the correct concentration and route. A 1 mg/mL (1:1000) preparation is used for IM anaphylaxis in many protocols; IV adrenaline is a specialist treatment for refractory shock or cardiac arrest and can cause fatal dosing errors. Always read the ampoule and follow local policy.

What not to do

Do not wait for rash, wheeze or a blood-pressure reading if the patient has sudden airway or breathing compromise after exposure.
Do not give antihistamine first while delaying adrenaline; antihistamines mainly improve itch and hives, not shock or airway oedema.
Do not use routine corticosteroids as a substitute for adrenaline; their onset is too slow to reverse acute airway or circulatory collapse.
Do not make a shocked patient stand, walk or sit upright suddenly.
Do not leave the patient alone after apparent recovery; biphasic reactions can occur.

6. Differential diagnosis of sudden collapse or wheeze

Look-alike	Clues	Important distinction
Severe asthma	Wheeze, chest tightness, previous asthma, no urticaria or trigger in some cases.	Asthma and anaphylaxis can coexist; treat suspected anaphylaxis with adrenaline and protocol-led bronchodilator.
Vasovagal syncope	Brief faint after pain/needle, pallor, bradycardia, rapid recovery when supine.	Persistent hypotension, wheeze, swelling or urticaria favours anaphylaxis.
Panic attack	Hyperventilation, fear, tingling, normal oxygenation and circulation.	Never label before checking ABCDE, glucose and exposure history.
Hereditary/bradykinin angioedema	Recurrent non-itchy swelling, abdominal pain, family history; often no urticaria.	Adrenaline may be less effective; airway planning and specialist therapy are urgent.
Sepsis or toxin	Fever, altered mental state, hypotension, exposure, abnormal glucose or pupils.	Continue resuscitation and source/toxin assessment; do not assume an allergy.

7. Angioedema and airway planning

Swelling of the tongue, floor of mouth or larynx can progress quickly. Ask about voice change, drooling, dysphagia, stridor and previous episodes. Sit the patient only if breathing requires it; prepare suction, oxygen and advanced airway support early. Histamine-mediated angioedema may accompany urticaria and respond to anaphylaxis treatment. Bradykinin-mediated angioedema, including ACE-inhibitor reactions, often lacks itch or hives and needs urgent airway and specialist management.

8. Severe cutaneous adverse reactions

Condition	Typical features	EMT priorities
Urticaria	Transient itchy wheals that move or fade; no mucosal injury.	Check for progression to anaphylaxis; document trigger and medicine exposure.
Serum sickness-like reaction	Fever, urticarial/morbilliform rash, joint pain, lymphadenopathy days after a medicine or infection.	Stop suspected medicine only with clinical direction, assess organ involvement and refer.
DRESS	Drug reaction with eosinophilia and systemic symptoms: fever, facial oedema, widespread rash, lymphadenopathy and liver/kidney injury.	Urgent hospital assessment; ask about anticonvulsants, antibiotics and all new medicines.
SJS/TEN	Painful dusky rash, bullae, epidermal detachment, mucosal erosions, fever and systemic illness.	Medical emergency: stop suspected drug under clinician direction, protect skin/eyes/airway, fluid/temperature support and urgent specialist care.
Fixed drug eruption	One or more sharply demarcated lesions recur at the same site after re-exposure.	Record the medicine and advise specialist review; extensive blistering needs emergency care.

9. Drug-allergy history that prevents harm

What exact medicine, formulation, route and dose caused the reaction?
How long after the dose did symptoms begin?
What symptoms occurred—itch, hives, swelling, wheeze, fainting, fever, blistering or organ injury?
Was the medicine stopped, and what treatment was required (adrenaline, ventilation, admission, ICU)?
Has the person tolerated related medicines since then?
Record a specific reaction, not just “allergy.” “Amoxicillin—anaphylaxis with wheeze and hypotension in 2024” is safer than “penicillin allergy.”

10. Antidote principles

Resuscitate first: airway, breathing, circulation, disability, exposure, glucose, temperature and ECG come before a named antidote.
Identify the toxin: agent, formulation, amount, route, time, co-ingestions, patient weight, pregnancy and kidney/liver disease.
Use a poison-centre or senior consultation: antidotes have indications, contraindications, dose limits and monitoring requirements.
Anticipate delayed toxicity: modified-release tablets, long half-life drugs, fat-soluble toxins and recurrent opioid respiratory depression can outlast early improvement.
Bring evidence: packets, bottles, photographs, pesticide labels and medication lists can be life-saving.
Document the response: time, route, dose, vital signs before/after, adverse reactions and the reason for repeating or stopping therapy.

11. High-yield antidotes for EMT revision

Toxin/clinical problem	Antidote or targeted treatment	Key cautions and monitoring
Opioids	Naloxone, titrated to restore adequate breathing rather than complete alertness.	Shorter duration than many opioids; recurrent respiratory depression, pulmonary oedema, pain and precipitated withdrawal. Continue ventilation and observation.
Paracetamol/acetaminophen	N-acetylcysteine (NAC) according to time, concentration and liver-risk protocol.	Do not wait for symptoms; an apparently well patient may develop delayed hepatic failure. Anaphylactoid reactions can occur during IV NAC.
Benzodiazepines	Flumazenil only in carefully selected cases with expert advice.	Can precipitate seizures, withdrawal and dysrhythmias in mixed overdose or dependence; airway support is usually safer.
Tricyclic antidepressants / sodium-channel blockade	Sodium bicarbonate under toxicology protocol.	Indicated for QRS widening, hypotension or ventricular dysrhythmia in appropriate poisonings; monitor pH, sodium, potassium and fluid status.
Organophosphate/carbamate cholinergic poisoning	Atropine; pralidoxime may be indicated for organophosphates.	Use PPE and decontamination. Titrate atropine to drying of bronchial secretions and improved ventilation, not pupil size alone; watch for delirium/hyperthermia.
Beta-blocker toxicity	Glucagon, high-dose insulin euglycaemic therapy, vasopressors and other specialist measures.	Bradycardia and shock may be profound; monitor glucose, potassium, ECG and fluid status continuously.
Calcium-channel blocker toxicity	IV calcium, high-dose insulin euglycaemic therapy, vasopressors and specialist support.	Hyperglycaemia, hypoglycaemia, hypokalaemia and myocardial dysfunction require serial monitoring.
Digoxin toxicity	Digoxin-specific antibody fragments (digoxin-Fab) when severe or indicated.	Arrhythmias and potassium shifts; do not delay specialist advice for a single level if unstable.
Warfarin	Vitamin K; four-factor PCC for life-threatening bleeding per protocol.	Balance thrombosis and bleeding risk; document INR, bleeding site and time of last dose.
Heparin	Protamine in selected significant bleeding.	Can cause hypotension/anaphylaxis and has dose limitations; resuscitation and surgical control may still be needed.
Methemoglobinaemia	Methylene blue when indicated; specialist consultation is essential.	Pulse oximetry may be misleading; risk of serotonin syndrome and haemolysis in G6PD deficiency.
Cyanide/smoke inhalation	Hydroxocobalamin and advanced supportive care per hazardous-exposure protocol.	Scene safety, decontamination and oxygenation; hydroxocobalamin causes red discoloration and can interfere with some tests.
Methanol/ethylene glycol	Fomepizole (or protocol-specific alternative), correction of acidosis and haemodialysis.	Visual symptoms, high anion/osmolar gap and renal injury may be delayed; urgent toxicology care.
Sulfonylurea hypoglycaemia	Dextrose plus octreotide under medical/toxicology direction.	Recurrent hypoglycaemia is common; monitor for many hours, especially with modified-release products.
Iron poisoning	Deferoxamine in severe poisoning.	GI symptoms, shock and metabolic acidosis; treatment requires hospital and laboratory monitoring.
Local anaesthetic systemic toxicity	20% lipid emulsion plus airway, seizure and cardiovascular support.	Stop local anaesthetic, call for resuscitation help and follow a lipid-rescue protocol.

12. Antidotes by toxidrome

Toxidrome	Pattern	Antidote/targeted support
Opioid	CNS depression, pinpoint pupils, slow/absent breathing, bradycardia.	Ventilation and naloxone; observe for recurrence.
Cholinergic	Salivation, lacrimation, urination, diarrhoea, vomiting, bronchorrhoea, bronchospasm, bradycardia, miosis and fasciculations.	PPE/decontamination, atropine, pralidoxime for organophosphate exposure, airway support.
Anticholinergic	Hot, dry skin, mydriasis, urinary retention, ileus, tachycardia, delirium.	Supportive care, temperature/ECG monitoring and specialist advice; avoid dangerous physical restraint.
Sympathomimetic	Agitation, sweating, mydriasis, tachycardia, hypertension, hyperthermia, seizures.	Quiet environment, benzodiazepine-led seizure/agitation control and cooling per protocol.
Sedative-hypnotic	Ataxia, slurred speech, CNS depression and hypoventilation.	Airway/ventilation and glucose; selective flumazenil only with expert advice.
Serotonergic	Agitation, clonus/hyperreflexia, tremor, diarrhoea, diaphoresis, hyperthermia.	Stop triggers, supportive care, cooling and urgent toxicology review.

13. Decontamination and exposure safety

Scene safety first: identify fumes, pesticides, contaminated clothing, powders, sharps and secondary exposure. Use gloves, eye protection and respiratory protection as trained.
Remove from exposure: fresh air for inhalation when safe, remove contaminated clothing and irrigate skin/eyes with copious clean water according to the chemical protocol.
Never induce vomiting: aspiration, burns and recurrent exposure can worsen injury. Do not give oral fluids or charcoal to a drowsy patient without a protected airway and expert advice.
Preserve information: keep the product container, photograph the label, estimate amount and record time and route.
Protect rescuers: a patient contaminated with pesticide or chemical can expose ambulance staff; request hazmat/decontamination support when required.

14. Special populations and antidote safety

Patient group	Extra considerations
Children	Weight-based calculations, accidental ingestion, smaller airway and rapid deterioration. Use paediatric concentrations and double-check arithmetic.
Pregnancy	Maternal oxygenation and circulation are priorities; do not withhold life-saving anaphylaxis or antidote treatment. Involve obstetric and toxicology teams.
Older adults	Polypharmacy, renal impairment, falls, frailty and atypical presentations. Start from physiology, not the medication list alone.
Asthma or cardiac disease	Adrenaline remains first-line for anaphylaxis; monitor rhythm and perfusion closely. Do not withhold it because of comorbidity.
Renal/hepatic disease	Longer toxin half-life and altered antidote clearance. Expect delayed toxicity and seek specialist dosing guidance.
Communication barriers	Use interpreters, accessible language and family/support persons with consent. Confirm exposure rather than relying on assumptions.

15. Clinical scenarios

Scenario 1 — Antibiotic reaction: Minutes after IV ceftriaxone, a patient develops hoarseness, wheeze, urticaria and dizziness. Stop the infusion, call for help, lay the patient appropriately, give IM adrenaline using the local concentration/protocol, support oxygenation and prepare transport. An antihistamine alone is inadequate.

Scenario 2 — ACE-inhibitor angioedema: A patient on enalapril has progressive tongue swelling and a muffled voice but no hives. Treat airway compromise as an emergency, give anaphylaxis therapy if clinically indicated, prepare early airway support and tell the receiving team that bradykinin-mediated angioedema is possible.

Scenario 3 — Pesticide exposure: A farm worker is sweating, vomiting, bradycardic, wheezing and has pinpoint pupils after spraying. Keep rescuers safe, remove contaminated clothing, irrigate as indicated, support ventilation and request urgent atropine/pralidoxime-led toxicology management.

Scenario 4 — Unknown tablets: An unconscious person has slow respirations and a packet of codeine plus diazepam. Ventilate, check glucose, administer naloxone when opioid toxicity is suspected and observe. Do not reflexively use flumazenil in a mixed overdose.

Scenario 5 — Paracetamol ingestion: A teenager feels well four hours after swallowing tablets. Do not reassure or discharge from the scene. Record the dose/time, bring the packet, check for co-ingestions and arrange urgent NAC assessment because liver injury can be delayed.

Scenario 6 — Painful blistering rash: A patient started carbamazepine ten days ago and now has fever, mucosal ulcers and skin tenderness. Suspect SJS/TEN, stop further exposure under medical direction, protect airway/skin/eyes and transfer urgently; do not treat as a simple allergy.

16. Handover and documentation template

Exposure: suspected agent, product/strength, dose estimate, route, time and co-exposures.
Reaction: first symptom, progression, skin/mucosa, airway, breathing, circulation, neurological findings and temperature.
Interventions: adrenaline/antidote name, concentration, route, dose, time, oxygen/ventilation, fluids, decontamination and response.
Measurements: serial vital signs, ECG rhythm/QRS/QTc, glucose, GCS/AVPU, urine output and relevant point-of-care tests.
Background: allergies, medicines, asthma, heart/kidney/liver disease, pregnancy, previous reactions and baseline function.
Safety: contamination risk to staff, safeguarding, intentional self-harm, means access and who was informed.

17. Revision questions

Why is IM adrenaline first-line in anaphylaxis while antihistamines and steroids are adjuncts?
List four airway or breathing signs that should trigger immediate anaphylaxis treatment.
How does bradykinin-mediated angioedema differ from histamine-mediated urticaria?
Why can a patient with severe anaphylaxis have no skin rash?
When might naloxone need to be repeated after apparent improvement?
Why is flumazenil hazardous in mixed overdose or benzodiazepine dependence?
Name three causes of cholinergic toxidrome and two targeted treatments.
Which antidote is used for significant paracetamol exposure and why should treatment not wait for symptoms?
What findings suggest SJS/TEN rather than simple urticaria?
What exposure and treatment details must appear in an antidote handover?

18. Key take-home points

Adrenaline is the life-saving first-line medicine for anaphylaxis with airway, breathing or circulation problems.
Position, oxygenation, ventilation, fluids, monitoring and rapid transport are as important as the antidote.
Antihistamines relieve itch/hives but do not reverse shock or upper-airway obstruction; routine steroids do not replace adrenaline.
Antidotes are toxin-specific, time-sensitive and potentially harmful; obtain expert advice and monitor the response.
Always consider mixed poisoning, delayed toxicity, recurrent respiratory depression and secondary contamination.
Record the exact reaction and suspected medicine so future care is safer and unnecessary “allergy” labels are avoided.

Selected authoritative resources

For EMT practice: When in doubt, return to ABCDE, remove further exposure, call for help, use the correct first-line treatment and keep reassessing. A precise timeline and clean handover can be as valuable as the medicine itself.

Hypersensitivity Reactions and Emergency Antidotes: Recognition, Use and Safety Read More »

Psychopharmacology: Mental Health Medicines, Emergency Uses and Safety

Why this matters in emergency medicine: Psychotropic medicines can restore function and prevent relapse, but they can also cause airway compromise, seizures, dysrhythmias, hyperthermia, severe hypotension, delirium and self-harm when misused. An EMT may be the first professional to recognise an adverse drug reaction, intentional overdose, withdrawal syndrome or a medical illness presenting as “psychiatric.” This guide links pharmacology to rapid assessment, safe transport, respectful communication and referral.

Scope and safety: These are learning notes, not a substitute for a prescriber, poison-centre advice, the Uganda Clinical Guidelines, local formularies or an emergency protocol. Never start, stop, combine or rapidly change a psychotropic medicine without the responsible clinician. In a deteriorating patient, use an ABCDE approach, call for senior/medical support early and treat life threats before making a diagnostic label.

Learning outcomes

Explain how major neurotransmitter systems relate to symptoms and medicine effects.
Classify antidepressants, antipsychotics, mood stabilisers, anxiolytics, hypnotics and medicines used in substance-related emergencies.
Recognise serotonin syndrome, neuroleptic malignant syndrome (NMS), acute dystonia, akathisia, tardive dyskinesia, lithium toxicity and severe withdrawal.
Perform a medication-focused history, risk assessment, monitoring plan and clear handover.
Support a person with agitation, psychosis, mania, self-harm or overdose without stigma, coercion or unsafe restraint.

1. What is psychopharmacology?

Psychopharmacology is the study of medicines that change mood, thinking, perception, behaviour, sleep, attention or impulse control. Medicines act at synapses by changing neurotransmitter release, receptor activity, reuptake or metabolism. Clinical response is usually slower than the plasma concentration change: sedation may occur after one dose, while antidepressant or antipsychotic benefit often takes days to weeks. This difference prevents premature dose escalation and helps the EMT explain why a patient may still be distressed despite taking treatment.

Emergency rule: A behavioural presentation is a symptom, not a diagnosis. Hypoglycaemia, hypoxia, hypercapnia, head injury, stroke, sepsis, meningitis, intoxication, withdrawal, thyroid disease and medication toxicity can all look like agitation, confusion or psychosis.

Core neurotransmitters and the bedside link

System	Main functions	Clinical relevance
GABA	Inhibitory “braking” of the CNS; muscle relaxation and anticonvulsant effect.	Benzodiazepines enhance GABA-A activity; excess causes drowsiness, hypoventilation, ataxia and coma. Withdrawal can cause tremor, anxiety, seizures and delirium.
Glutamate	Major excitatory transmitter; learning, memory and arousal.	Excess excitotoxicity is relevant in seizures and injury; NMDA antagonism contributes to ketamine dissociation and analgesia.
Dopamine	Movement, reward, attention and salience.	Excess mesolimbic activity is associated with hallucinations/delusions; blockade can cause parkinsonism, dystonia, akathisia and NMS.
Serotonin (5-HT)	Mood, anxiety, sleep, appetite, gut motility and temperature regulation.	SSRIs/SNRIs increase signalling; combinations or overdose may produce serotonin syndrome.
Noradrenaline	Alertness, arousal, attention, vascular tone and stress response.	SNRIs and some TCAs increase it; toxicity can cause hypertension, tachycardia, agitation and dysrhythmia.
Acetylcholine	Memory, attention, autonomic and neuromuscular function.	Anticholinergic effects cause dry mouth, blurred vision, urinary retention, ileus, tachycardia and delirium.
Histamine	Wakefulness, appetite and itch.	H1 blockade explains sedation and weight gain with some antipsychotics and antidepressants.

2. Classification used in emergency care

Group	Examples	Typical roles	Emergency hazards
Antidepressants	SSRIs: fluoxetine, sertraline, escitalopram; SNRIs: venlafaxine, duloxetine; TCAs: amitriptyline; others: mirtazapine, bupropion, MAOIs.	Depression, anxiety disorders, OCD, PTSD, neuropathic pain (some agents).	Serotonin syndrome, withdrawal, seizures, QT/QRS abnormalities and coma in overdose.
Antipsychotics	First generation: haloperidol, chlorpromazine. Second generation: risperidone, olanzapine, quetiapine, aripiprazole, clozapine.	Psychosis, schizophrenia, mania, severe agitation; some bipolar depression.	Acute dystonia, akathisia, NMS, QT prolongation, hypotension, aspiration and metabolic disease.
Mood stabilisers	Lithium, valproate, carbamazepine, lamotrigine.	Bipolar mania or maintenance; seizure disorders; selected bipolar depression.	Narrow therapeutic index, renal/hepatic toxicity, blood dyscrasias, teratogenicity and serious rash.
Anxiolytics/sedatives	Diazepam, lorazepam, midazolam; buspirone; selected hypnotics.	Severe anxiety, seizures, alcohol withdrawal, procedural sedation.	Respiratory depression, aspiration, paradoxical agitation, falls, dependence and withdrawal.
Substance-use medicines	Naloxone, methadone/buprenorphine programmes, acamprosate, naltrexone, thiamine protocols.	Overdose reversal, withdrawal prevention and relapse reduction.	Precipitated withdrawal, respiratory depression, QT prolongation or missed Wernicke prophylaxis.

3. Safe psychotropic medicine principles

Confirm the person and the product: name, strength, formulation, route, time of last dose, indication, prescriber and adherence.
Check the context: new medicine, dose increase, missed doses, recent infection, dehydration, pregnancy, alcohol/recreational drugs, over-the-counter medicines and herbal products.
Use one change at a time where possible: simultaneous changes make adverse effects and therapeutic response difficult to interpret.
Do not abruptly stop long-term therapy: withdrawal or relapse can be dangerous; tapering is planned by the treating clinician.
Monitor physiology, not just behaviour: airway, respiratory rate, oxygen saturation, pulse, blood pressure, temperature, glucose, ECG, level of consciousness and hydration.
Use the least restrictive safe approach: verbal de-escalation, a calm environment and trained staff precede medication or restraint unless there is immediate life-threatening violence.

4. Antidepressants

Antidepressants are used for depressive disorders and several anxiety-related conditions. They are not “happy pills”: benefit requires a therapeutic trial, adherence and psychological/social support. Early activation, insomnia, nausea or anxiety may occur before mood improves. In a young person or anyone with new suicidal thoughts, arrange urgent review rather than simply increasing the dose.

SSRIs and SNRIs

Feature	SSRIs	SNRIs
Examples	Fluoxetine, sertraline, citalopram, escitalopram, paroxetine.	Venlafaxine, duloxetine, desvenlafaxine.
Common effects	Nausea, loose stool, headache, insomnia or somnolence, sexual dysfunction.	SSRI effects plus sweating, tremor, increased pulse or blood pressure.
Important interactions	Other serotonergic drugs, tramadol, linezolid, MAOIs, some migraine medicines and herbal St John’s wort.	Same serotonergic risk; medicines affecting blood pressure require caution.
Withdrawal	Dizziness, “electric shock” sensations, irritability, flu-like symptoms, sleep disturbance.	Often more prominent with short half-life drugs; taper under clinician guidance.
EMT priority	Ask about a recent switch or combination; screen for serotonin syndrome, mania, overdose, self-harm and severe hyponatraemia symptoms.

Serotonin syndrome — “HOT, WET, SHAKY, FAST”: hyperthermia, diaphoresis, diarrhoea, agitation/confusion, tremor, hyperreflexia/clonus, tachycardia and hypertension. It is a clinical emergency: stop suspected serotonergic agents as directed, begin ABCDE, cool safely, manage seizures/agitation per protocol and arrange urgent medical/poison-centre support.

Tricyclic antidepressants (TCAs)

Amitriptyline, imipramine and related TCAs block reuptake of noradrenaline and serotonin but also block muscarinic, histamine and alpha-1 receptors. This explains their anticholinergic effects, sedation, postural hypotension and high toxicity in overdose. A patient with a possible TCA overdose requires immediate ECG and continuous monitoring; QRS widening, hypotension, ventricular dysrhythmia, seizures or reduced consciousness are red flags. Sodium bicarbonate and advanced management are clinician-led under the local toxicology protocol.

MAOIs and other antidepressants

MAOIs: dangerous interactions with serotonergic medicines, sympathomimetics and tyramine-rich foods; severe headache, hypertension, hyperthermia or agitation needs urgent care.
Mirtazapine: sedation and increased appetite are common; overdose is often less cardiotoxic than TCAs but still requires assessment.
Bupropion: may lower seizure threshold; repeated or modified-release overdose can cause delayed seizures and dysrhythmias.
Ketamine/esketamine: specialist use only; monitor airway, blood pressure, dissociation and emergence reactions.

5. Antipsychotic medicines

Antipsychotics reduce dopamine signalling to treat hallucinations, delusions, severe thought disorder and mania. They do not replace a search for delirium, intoxication, withdrawal, hypoxia, hypoglycaemia, infection or neurological disease. Second-generation agents may have less movement toxicity for some patients but can cause major metabolic, cardiac and sedation effects.

Class/agents	Practical strengths	Major adverse effects	EMT observations
First generation: haloperidol, chlorpromazine	Useful for psychosis or severe agitation when prescribed; haloperidol has relatively little anticholinergic sedation.	Dystonia, akathisia, parkinsonism, tardive dyskinesia, NMS, QT prolongation; chlorpromazine can cause marked hypotension.	Check temperature, rigidity, pulse, ECG risk, hydration and co-administered QT-prolonging drugs.
Risperidone, paliperidone	Psychosis and maintenance; long-acting formulations support adherence.	Extrapyramidal symptoms, raised prolactin, orthostasis and QT risk.	Ask about rigidity, tremor, menstrual/sexual effects and recent depot injection.
Olanzapine, quetiapine	Psychosis and bipolar illness; quetiapine is sedating.	Weight gain, diabetes, dyslipidaemia, postural hypotension, sedation; QT risk.	Protect airway when drowsy; check glucose and falls risk.
Aripiprazole	Partial dopamine agonist; often less sedating and less metabolic effect.	Akathisia, insomnia, nausea and impulse-control problems.	Restlessness may be akathisia, not worsening psychosis—ask before giving more sedative.
Clozapine	Specialist treatment for treatment-resistant schizophrenia and reduction of recurrent suicidal behaviour in selected patients.	Neutropenia/agranulocytosis, myocarditis, seizures, severe constipation/ileus, hypersalivation, metabolic effects and sedation.	Fever, sore throat, infection, chest pain, breathlessness, abdominal distension or collapse is urgent; never interrupt monitoring casually.

Extrapyramidal syndromes

Syndrome	Typical timing/findings	Immediate EMT response
Acute dystonia	Hours–days: painful neck spasm, jaw/tongue protrusion, oculogyric crisis, dysphagia or laryngospasm.	Airway first; call for urgent treatment with an anticholinergic/antihistamine per protocol. Do not assume seizure or “bad behaviour.”
Akathisia	Days–weeks: inner restlessness, pacing, inability to sit still, anxiety and sometimes suicidal distress.	Ask directly about restlessness; notify prescriber. More antipsychotic may worsen it.
Parkinsonism	Weeks–months: bradykinesia, rigidity, resting tremor, shuffling gait.	Falls precautions and medication review; do not stop abruptly without a plan.
Tardive dyskinesia	Months–years: repetitive lip smacking, tongue movements, chewing or choreiform limb movements.	Document and refer; avoid dismissing it as anxiety. Long-term specialist treatment may be required.
NMS	Rapid rigidity, hyperthermia, altered consciousness, autonomic instability and raised CK after dopamine blockade or withdrawal of dopaminergic drugs.	Life-threatening emergency: stop suspected trigger under medical direction, ABCDE, active cooling, IV access/fluids and urgent critical-care referral.

NMS versus serotonin syndrome: NMS usually develops over days with “lead-pipe” rigidity, bradyreflexia and a dopamine-blocking exposure; serotonin syndrome often develops rapidly after serotonergic exposure with clonus, hyperreflexia, tremor, diarrhoea and diaphoresis. There can be overlap—treat the patient’s physiology and seek specialist help rather than relying on a single sign.

6. Mood stabilisers

Mood stabilisers reduce recurrence of mania and depression in bipolar disorder and may be used for seizure disorders. They require adherence, laboratory monitoring and a clear plan for pregnancy, renal/hepatic disease and drug interactions. WHO guidance supports lithium, valproate or carbamazepine for bipolar mania where appropriate; lithium should be initiated only where close clinical and laboratory monitoring is available. Maintenance choices are individualised and should be continued long enough to prevent relapse unless toxicity or another contraindication occurs.

Lithium

Topic	Teaching and emergency significance
How it is used	Acute mania and bipolar maintenance; a narrow therapeutic index means the effective and toxic concentrations are close.
Monitoring	Serum level at the correct time after dosing, renal function, electrolytes, thyroid function, weight, hydration and pregnancy status where relevant.
Why levels rise	Dehydration, vomiting/diarrhoea, fever, low-salt diet, acute kidney injury and interacting medicines such as NSAIDs, ACE inhibitors/ARBs and thiazide diuretics.
Early toxicity	Nausea, diarrhoea, coarse tremor, thirst, polyuria, weakness, ataxia, slurred speech and increasing confusion.
Severe toxicity	Marked tremor, hyperreflexia, seizures, reduced consciousness, dysrhythmia or renal failure. Do not induce vomiting; withhold further doses pending urgent clinician/poison-centre advice and support ABCDE.
Patient education	Keep fluid and salt intake steady, avoid unsupervised NSAIDs, report persistent vomiting/diarrhoea or fever, and never double a missed dose without advice.

Valproate (sodium valproate/valproic acid)

Used for mania and epilepsy; common effects include nausea, tremor, sedation, weight gain and hair changes.
Serious toxicity includes hepatotoxicity, pancreatitis, thrombocytopenia, hyperammonaemic encephalopathy and coma.
Check for abdominal pain, persistent vomiting, jaundice, bruising, confusion or reduced consciousness; arrange urgent laboratory review.
It carries major fetal risk. It should not be used for bipolar maintenance in women and girls of childbearing potential where safer effective alternatives are available; pregnancy decisions require specialist review, not abrupt stopping.

Carbamazepine and lamotrigine

Medicine	Key cautions	Red flags for urgent referral
Carbamazepine	Diplopia, ataxia, hyponatraemia, hepatic injury, leukopenia, aplastic anaemia, rash and multiple interactions through enzyme induction.	Seizure, severe ataxia, confusion, syncope, mucosal rash, fever/sore throat, jaundice or overdose.
Lamotrigine	Slow titration is essential; missed doses may require re-titration. Interaction with valproate increases lamotrigine exposure.	Any blistering rash, mucosal ulceration, facial oedema, fever or systemic illness suggests Stevens–Johnson syndrome/toxic epidermal necrolysis.

“LITHIUM = RENEW”: Renal function, Electrolytes/fluid balance, Neurological signs, Endocrine/thyroid, Warnings from interacting medicines. A normal-looking patient can deteriorate after dehydration or a new NSAID.

7. Anxiolytics, hypnotics and sedative medicines

Benzodiazepines (diazepam, lorazepam, midazolam and related agents) enhance GABA-A activity. They can be lifesaving for prolonged seizures, severe alcohol withdrawal and carefully monitored procedural sedation. They are also common causes of falls, aspiration, respiratory depression, dependence and difficult withdrawal. The danger increases when combined with opioids, alcohol, sedating antihistamines or other CNS depressants.

Situation	What the EMT should look for	Safety action
Therapeutic sedation	Increasing drowsiness, reduced airway tone, slow/shallow breathing, hypotension.	Continuous observation, oxygen/ventilation readiness, suction and reversal/advanced support according to local protocol.
Benzodiazepine overdose	Ataxia, slurred speech, somnolence, hypoventilation or coma; mixed ingestion is common.	ABCDE and glucose; protect airway. Flumazenil is not routine and may precipitate seizures or withdrawal in dependent patients or mixed TCA overdose.
Alcohol withdrawal	Tremor, sweating, anxiety, tachycardia, hypertension, hallucinations, seizures or delirium tremens.	Urgent medical care, glucose/thiamine considerations, calm environment, seizure precautions and protocol-led benzodiazepine treatment.
Withdrawal after long use	Rebound anxiety/insomnia, tremor, perceptual changes, seizures and delirium.	Never advise abrupt cessation; communicate the last dose and arrange supervised tapering.

8. Acute agitation, psychosis and mania

Agitation ranges from anxiety and pacing to excited delirium-like states with immediate danger. Treat the person as medically unwell until reversible causes are considered. A calm approach is clinically effective and preserves dignity.

A practical emergency sequence

Make the scene safe: remove weapons and bystanders, keep an exit route, use trained staff and request security/police support only for safety—not punishment.
Introduce and listen: one lead communicator, short sentences, non-threatening posture, respectful name/pronouns and validation of distress without agreeing with delusions.
Rapid medical screen: airway, breathing, circulation, glucose, temperature, oxygen saturation, trauma, toxidromes, infection, pain, urinary retention and medication/withdrawal history.
Offer choices: quiet room, trusted relative, oral medicine if prescribed and accepted, or transport for assessment. Explain what will happen.
Escalate early: senior clinician, mental-health team, toxicology or critical care if violence, severe psychosis, delirium, hyperthermia, hypoxia, seizure, intoxication or self-harm risk is present.
Monitor after any sedative: respiratory rate, SpO2, pulse, blood pressure, temperature, level of consciousness, ECG where indicated and the time/dose/route of every medicine.

Never diagnose delirium as “psychiatric.” New fluctuating inattention, disorientation, visual hallucinations, fever, abnormal vital signs or altered consciousness suggests a medical/toxic cause and needs urgent investigation.

9. Medicines in substance-related emergencies

Opioid toxicity and naloxone

Suspect opioid toxicity in a person with pinpoint pupils, reduced consciousness and slow or absent breathing. Call for help, open the airway, provide rescue ventilation/oxygen and give naloxone according to the available local protocol. Naloxone may wear off before a long-acting opioid; recurrent respiratory depression requires observation and repeat treatment by trained clinicians. Sudden awakening can produce vomiting, agitation, pain and acute withdrawal—protect the patient and staff while continuing to monitor breathing.

Alcohol and sedative withdrawal

Withdrawal can be fatal. Ask when alcohol or sedatives were last used, previous withdrawal seizures/delirium, daily quantity and co-use of opioids. Tremor, autonomic instability, hallucinations, seizures or confusion requires urgent medical management. Do not give an isolated sedative dose without monitoring and a protocol.

10. Intentional overdose and self-harm

Use a non-judgmental, private approach. Ask directly whether the ingestion was intentional, what was taken, how much, when, and whether other substances were involved. Bring packets, bottles, prescriptions or photographs. Do not wait for symptoms: some medicines have delayed cardiotoxicity, seizures, liver injury or serotonin/NMS complications.

Priority	Action
Immediate threats	ABCDE, glucose, temperature, oxygen saturation, ECG, IV access where trained, seizure precautions and poison-centre/medical consultation.
Decontamination	Do not induce vomiting. Activated charcoal or other decontamination is clinician/poison-centre-led and depends on timing, substance, airway protection and contraindications.
Risk and safeguarding	Ask about ongoing suicidal intent, access to medicines/weapons, violence, dependants, pregnancy and whether the person is safe to leave. Maintain observation and remove immediate means.
Handover	State exact agent, formulation, dose estimate, time, co-ingestions, symptoms, vital trends, ECG findings, treatment and response.

11. Suicide-risk communication and safety planning

Ask clearly: “Have you wished you were dead?”, “Have you thought about killing yourself?”, “Do you have a plan, access to the means and an intention to act?” Asking does not create suicidal thoughts; it identifies danger. Listen without arguing, promise only what you can deliver, involve a trusted support person with consent where safe, and arrange urgent mental-health assessment for current intent, recent attempt, severe depression, psychosis, intoxication, inability to collaborate or lack of a safe environment.

Safety-plan essentials: warning signs; internal coping strategies; people and places that provide distraction; trusted people to contact; professional/crisis contacts; and practical removal or restriction of medicines, pesticides, weapons and other lethal means. Document who will supervise medicines and when follow-up will occur.

12. High-risk adverse reactions: recognition and first actions

Reaction	Clues	What to do now
Serotonin syndrome	Recent serotonergic combination or overdose; agitation, sweating, diarrhoea, tremor, clonus/hyperreflexia, fever and tachycardia.	ABCDE, stop suspected agents under medical direction, remove excess heat, IV/monitoring support and urgent senior/toxicology review.
Neuroleptic malignant syndrome	Dopamine blocker; lead-pipe rigidity, hyperthermia, altered consciousness, autonomic instability and raised CK.	Emergency transfer, cooling, airway/ventilation readiness, fluids and critical-care management.
Acute dystonia	Oculogyric crisis, torticollis, jaw spasm, dysphagia or laryngospasm after antipsychotic/antiemetic.	Airway assessment and urgent protocol-led anticholinergic treatment.
Severe akathisia	Subjective inner torment and pacing soon after antipsychotic change; may mimic anxiety or worsening psychosis.	Do not dismiss or automatically escalate antipsychotic; urgent prescriber review and suicide-risk screen.
Anticholinergic delirium	Hot, dry skin, dilated pupils, tachycardia, urinary retention, ileus, hallucinations and confusion.	ABCDE, temperature/ECG/glucose, cooling and toxicology/medical advice; avoid physical struggle if possible.
Severe hyponatraemia	Headache, nausea, confusion, seizures or reduced consciousness; possible with SSRIs, carbamazepine or diuretics.	Seizure precautions and urgent medical/laboratory management; do not rapidly correct without protocol.
Clozapine-related infection/myocarditis	Fever, sore throat, malaise, chest pain, dyspnoea, palpitations or unexplained tachycardia.	Urgent medical review, FBC/inflammatory/cardiac tests as directed and do not assume a benign viral illness.

13. Medication history for the psychiatric emergency

Question	Why it changes care
What medicines, strengths and formulations are taken?	Identifies long-acting injections, modified-release products, high-risk agents and duplicate therapy.
When was the last dose? Any missed doses or recent changes?	Separates withdrawal, relapse, adverse effect and delayed toxicity.
Any alcohol, opioids, stimulants, cannabis or herbal products?	Mixed intoxication/withdrawal changes airway, seizure and interaction risk.
Kidney, liver, heart, epilepsy, diabetes or pregnancy?	Changes clearance, QT risk, metabolic monitoring and medicine choice.
Previous reactions or suicide attempts?	Predicts recurrence and informs safe transport, observation and safeguarding.
Who prescribes and where are records?	Enables accurate reconciliation and prevents unsafe duplication or abrupt interruption.

14. Special populations

Children and adolescents: use weight-appropriate, protocol-led dosing; assess safeguarding, developmental context, accidental ingestion and emerging suicidal thoughts. Avoid adult assumptions.
Older adults: start low and monitor slowly; renal impairment, falls, delirium, anticholinergic burden and QT prolongation are common hazards.
Pregnancy and breastfeeding: do not abruptly stop effective treatment. Rapidly involve obstetric and mental-health clinicians; valproate has major fetal risk and lithium needs specialist risk–benefit monitoring.
Renal or hepatic disease: reduced clearance can turn a normal dose into toxicity. Ask for recent creatinine/LFTs and report the condition in handover.
People with disabilities or communication barriers: use accessible language, hearing/visual aids, a support person and behavioural baseline; do not mistake communication differences for psychosis.
People experiencing homelessness or poverty: treatment adherence may be limited by food, transport, storage and safety. Link to social and community services rather than labelling “non-compliant.”

15. Common interactions worth remembering

Combination/problem	Potential harm	EMT teaching point
SSRI/SNRI + MAOI, linezolid, tramadol, lithium or St John’s wort	Serotonin syndrome.	Ask specifically about new antibiotics, analgesics and herbal products.
Lithium + NSAID, ACE inhibitor/ARB or thiazide	Raised lithium concentration and toxicity.	Dehydration plus a “routine” pain medicine can be the trigger.
Antipsychotic + other QT-prolonging medicine or hypokalaemia	Torsades de pointes and syncope.	ECG and electrolyte review are important before/after emergency sedation.
Opioid + benzodiazepine/alcohol	Synergistic respiratory depression and death.	Prioritise breathing; provide naloxone/ventilation according to protocol.
Valproate + lamotrigine	Increased lamotrigine exposure and severe rash risk.	Any mucosal or blistering rash is an emergency.
Clozapine + smoking cessation or infection	Metabolic changes can raise clozapine exposure and toxicity.	Report sudden smoking change, fever, seizures, sedation or constipation.

16. Clinical scenarios for EMT students

Scenario 1 — “The restless patient after a dose increase”: A patient on risperidone paces continuously, says they cannot keep still and has new suicidal thoughts. Vital signs are stable. Consider akathisia rather than “non-cooperation”; maintain safety, ask about self-harm, notify the prescriber and document the recent dose change.

Scenario 2 — “Hot and rigid”: A patient treated with haloperidol develops 40°C temperature, severe rigidity, confusion and tachycardia. Treat as NMS until proved otherwise: ABCDE, urgent transfer, cooling, IV/critical-care support and immediate medication review.

Scenario 3 — “Vomiting on lithium”: A patient with bipolar disorder has diarrhoea, coarse tremor, ataxia and slurred speech after several days of poor intake and ibuprofen use. Suspect lithium toxicity, protect from falls, withhold further unsupervised doses, bring the medication packet and seek urgent laboratory/toxicology advice.

Scenario 4 — “Several serotonergic tablets”: After taking an SSRI with tramadol, a patient has agitation, sweating, tremor and inducible clonus. Manage airway/breathing/circulation, temperature and seizures, stop further serotonergic exposure under clinician direction and arrange urgent toxicology care.

Scenario 5 — “Psychosis with low glucose”: A confused, shouting patient has a glucose of 2.4 mmol/L. Correct the life threat under protocol and reassess before labelling the behaviour psychosis. A medical cause can coexist with a psychiatric history.

17. Documentation and handover checklist

Baseline mental state, orientation, speech, behaviour, risk statements and capacity/consent where relevant.
Exact medicine names, strengths, formulation, route, prescribed dose, last dose, missed doses, allergies and recent changes.
Alcohol/recreational drug history, pregnancy possibility, kidney/liver/heart disease, epilepsy, diabetes and previous adverse reactions.
Vital-sign trends, glucose, temperature, oxygen saturation, ECG findings, neurological signs, fluid intake/output and injury assessment.
De-escalation attempted, who was present, medicines administered (time/route/dose), response and adverse effects.
Suicide/violence/self-neglect risk, access to means, safeguarding concerns, family/support person and agreed safety plan.
Destination, receiving clinician, advice received and exact time of handover.

18. Patient and family education

Explain the purpose of each medicine in plain language and state when benefit is expected.
Give a simple missed-dose plan from the prescriber/pharmacist; never “catch up” by doubling without advice.
Explain which symptoms require urgent help: breathing difficulty, collapse, severe rash, fever/rigidity, seizures, fainting, severe confusion, suicidal intent, jaundice, chest pain or persistent vomiting.
Encourage one pharmacy/medicine list and safe storage away from children and anyone at risk of overdose.
Warn against mixing sedatives with alcohol or opioids and against sharing prescribed medicines.
For lithium and other monitored drugs, keep appointments for blood tests and report dehydration, new medicines or major diet/fluid changes.

Exam and practice point: A normal blood pressure does not make a sedated patient safe. Airway tone and ventilation may deteriorate before the monitor alarm. Reassess after every intervention and after every change in consciousness.

19. Quick comparison: when to suspect which emergency?

Presentation	Most useful clues	Priority
Agitated + sweaty + clonus	Serotonergic drug/interaction, hyperreflexia, diarrhoea.	Serotonin syndrome; ABCDE, cooling, urgent toxicology.
Agitated + rigid + very hot	Dopamine blocker, lead-pipe rigidity, autonomic instability.	NMS; emergency transfer and critical-care support.
Drowsy + slow breathing	Opioid, benzodiazepine, alcohol or mixed ingestion.	Airway/ventilation, glucose, naloxone where opioid toxicity suspected.
Confused + dry + dilated pupils	Anticholinergic medicines, urinary retention, ileus, tachycardia.	Toxicological emergency; ECG, temperature and medical review.
Tremor + diarrhoea + ataxia	Lithium exposure, dehydration, NSAID/ACE inhibitor/thiazide use.	Withhold further unsupervised doses and obtain urgent level/renal assessment.
New psychosis + fluctuating attention	Delirium, infection, hypoxia, glucose/electrolyte problem or intoxication.	Search for a medical cause; do not treat as primary psychosis alone.

20. Revision questions

Why can a patient with serotonin syndrome have clonus and diarrhoea while a patient with NMS has marked rigidity?
List four factors that can increase lithium concentration and name four early toxicity findings.
What are the first five actions when a person is severely agitated in the ambulance bay?
Why is flumazenil not a routine antidote for every benzodiazepine overdose?
Which antipsychotic adverse effect presents as painful neck spasm or oculogyric crisis?
Why must glucose and oxygenation be checked before diagnosing a behavioural emergency?
What information must accompany a handover after intentional psychotropic ingestion?
How does an EMT distinguish akathisia from “worsening psychosis”?
What counselling is important for a patient taking valproate who may become pregnant?
Describe the components of a practical safety plan after self-harm.

21. Key take-home points

Psychiatric symptoms can be caused or amplified by hypoxia, glucose/electrolyte disturbance, infection, trauma, intoxication, withdrawal or medicine toxicity.
Antidepressants need time and monitoring; combinations can cause serotonin syndrome and abrupt cessation can cause withdrawal.
Antipsychotics can cause movement disorders, QT prolongation, metabolic disease and life-threatening NMS.
Lithium is effective but unforgiving: hydration, renal function, salt balance and interactions matter.
Valproate, carbamazepine and lamotrigine require liver/blood/rash and pregnancy safety vigilance.
Benzodiazepines can save lives in seizures and withdrawal but can suppress breathing, especially with opioids or alcohol.
Respectful de-escalation, least-restrictive care, direct suicide questions and careful documentation are core emergency skills.

Selected authoritative learning resources

WHO Mental Health Gap Action Programme (mhGAP) — evidence-based guidance for non-specialist settings.
WHO psychosis and bipolar evidence centre — antipsychotics and mood-stabiliser recommendations.
NICE psychosis and schizophrenia guideline — antipsychotic choice, monitoring and clozapine.
WHO self-harm and suicide evidence — safety planning and follow-up.

For EMT practice: Treat every medicine as both a therapeutic tool and a potential source of harm. A calm voice, complete medication history, repeated physiological assessment and early senior consultation prevent more deaths than a rushed label.

Psychopharmacology: Mental Health Medicines, Emergency Uses and Safety Read More »

Musculoskeletal Medicines: Analgesics, Arthritis, Gout and Bone Safety

Why this topic matters in emergency medical care

Musculoskeletal medicines span acute pain relief, inflammation control, fracture care, gout flares, osteoporosis and autoimmune disease. EMTs must relieve suffering without worsening bleeding, kidney injury, respiratory depression or occult fracture. A hot swollen joint may be gout, septic arthritis or haemarthrosis; a “simple” back pain may be spinal cord compression. Safe medicine use begins with examination, mechanism and red-flag recognition.

This lesson supports EMT and nursing learning. Use current Uganda Ministry of Health guidance, local protocols, prescriber orders and patient-specific contraindication checks in practice.

Learning outcomes

Classify non-opioid/opioid analgesics, NSAIDs, corticosteroids, DMARDs, gout medicines, muscle relaxants and bone medicines.
Explain mechanisms, onset, routes, adverse effects, interactions and monitoring for each major class.
Recognise fracture, compartment syndrome, septic arthritis, spinal cord compression, cauda equina syndrome and neurovascular compromise.
Apply safe pain assessment, immobilisation, renal/GI/bleeding precautions and reassessment after analgesia.
Understand long-term medicines for rheumatoid arthritis, osteoarthritis, gout, osteoporosis and inflammatory disease.

1. Musculoskeletal physiology and medicine targets

Target	Effect	Medicine examples	Emergency relevance
Cyclo-oxygenase/prostaglandins	Pain, inflammation, fever, gastric and renal protection	NSAIDs, aspirin	Analgesia and anti-inflammatory effect balanced against ulcer, bleeding and AKI.
Opioid receptors	Central/peripheral analgesia and respiratory drive	Morphine, fentanyl, tramadol, naloxone	Severe pain relief but monitor ventilation and mental state.
Glucocorticoid receptors	Suppress inflammatory gene transcription	Prednisolone, dexamethasone, intra-articular steroids	Rapid anti-inflammatory effect; infection, hyperglycaemia and adrenal suppression risks.
Urate crystal/inflammation pathways	Neutrophil activation in gout	Colchicine, NSAID, corticosteroid, allopurinol	Acute flare treatment differs from long-term urate lowering.
Bone resorption/remodelling	Osteoclast and osteoblast balance	Bisphosphonates, denosumab, teriparatide, calcium/vitamin D	Fragility fracture prevention; hypocalcaemia and jaw/renal precautions.

2. Practical classification of musculoskeletal medicines

Group	Examples	Main role	Major concern
Paracetamol	Paracetamol/acetaminophen	Mild–moderate pain and fever	Liver toxicity in overdose or malnutrition/alcohol disease
NSAIDs	Ibuprofen, diclofenac, naproxen, ketorolac	Inflammatory pain, renal colic, gout	GI bleed, AKI, hypertension, heart failure and bronchospasm
Opioids	Morphine, fentanyl, codeine, tramadol	Moderate–severe acute pain	Respiratory depression, sedation, dependence and constipation
DMARDs	Methotrexate, hydroxychloroquine, sulfasalazine, leflunomide	Rheumatoid/inflammatory arthritis disease control	Immunosuppression, liver/blood toxicity and pregnancy warnings
Gout medicines	Colchicine, allopurinol, febuxostat	Acute flare and long-term urate lowering	Colchicine toxicity and incorrect initiation during acute illness
Bone medicines	Alendronate, zoledronic acid, denosumab, calcium/vitamin D	Osteoporosis and fracture prevention	Hypocalcaemia, renal impairment, oesophagitis and rare jaw problems

3. Paracetamol and multimodal analgesia

Paracetamol is useful for many acute pain presentations and can be combined with an NSAID or opioid. It has a ceiling effect, so repeating extra doses does not provide unlimited relief. Ask about combination cold/flu products, alcohol, malnutrition, liver disease and the total dose in the previous 24 hours.

Record weight and cumulative dose before giving another dose.
Suspected overdose, staggered ingestion or intentional self-harm requires urgent assessment even when the patient feels well.
Analgesia should accompany immobilisation, elevation, ice when appropriate and treatment of the underlying injury.

4. Non-steroidal anti-inflammatory drugs

Benefit	Mechanism	Important harm	Use caution/avoid
Reduce inflammatory pain	COX inhibition reduces prostaglandins	Dyspepsia, ulcer and GI bleeding	Previous ulcer, anticoagulation, steroid use or active bleeding
Relieve renal colic/gout	Suppresses inflammation and ureteric prostaglandins	AKI and sodium/fluid retention	Dehydration, CKD, shock, heart failure or pregnancy restrictions
Reduce fever/swelling	Peripheral anti-inflammatory action	Bronchospasm in aspirin-sensitive asthma	Previous NSAID reaction or uncontrolled asthma
Topical NSAID	Local exposure with lower systemic levels	Skin reactions and some systemic absorption	Broken skin, allergy and extensive use

Use the lowest effective dose for the shortest duration and consider gastroprotection when risk is high. NICE recommends NSAIDs as one first-line option for acute gout and as first-line analgesia for suspected renal colic when not contraindicated; patient-specific renal, GI and cardiovascular risk remains decisive.

5. Opioid analgesics and emergency monitoring

Medicine	Useful feature	Major risk	Monitoring
Morphine	Strong titratable analgesia	Hypoventilation, hypotension, nausea and histamine release	Respiratory rate, SpO2, ventilation, BP, GCS and pain score
Fentanyl	Rapid potent analgesia with less histamine	Apnoea, chest-wall rigidity, bradycardia	Continuous observation; prepare ventilation and naloxone.
Codeine	Oral mild–moderate pain option	Variable metabolism, sedation and constipation	Check respiratory disease, age and other sedatives.
Tramadol	Opioid plus serotonin/noradrenaline action	Seizure and serotonin syndrome risk	Ask about antidepressants, epilepsy and renal function.

5.1 Opioid safety checklist

Assess pain, airway, breathing, circulation, mental state and cause of pain before dosing.
Check allergies, opioid tolerance, alcohol/benzodiazepines, sleep apnoea, renal/hepatic disease and pregnancy.
Use the lowest authorised dose and titrate; do not repeat without a timed reassessment.
Monitor ventilation—not only oxygen saturation—because supplemental oxygen can conceal hypoventilation.
Have suction, bag-mask ventilation and naloxone access when giving parenteral opioid.

6. Muscle relaxants and spasm medicines

Muscle relaxants may reduce spasm but can cause sedation, hypotension, anticholinergic effects and falls. They should not delay examination for fracture, compartment syndrome, meningitis or spinal cord compression. Avoid combining sedating muscle relaxants with opioids or alcohol without close monitoring.

7. Osteoarthritis medicines

Osteoarthritis affects the whole joint and is managed with exercise, strengthening, weight support, education and selected medicines. NICE does not recommend routine paracetamol or weak opioids when alternatives are appropriate; topical NSAIDs may be useful for knee/hand disease, while oral NSAIDs require risk assessment.

Option	Role	Safety point
Topical NSAID	Local pain/inflammation relief	Check skin integrity and allergy; systemic absorption still occurs.
Oral NSAID	Short-term pain/inflammation when appropriate	Consider GI protection and renal/cardiovascular contraindications.
Intra-articular corticosteroid	Short-term relief for selected joints	Exclude infection first; monitor glucose and post-injection infection.
Opioid	Only selected severe pain when other measures unsuitable	Falls, dependence, constipation and respiratory depression.

8. Rheumatoid arthritis and DMARDs

Rheumatoid arthritis is systemic autoimmune inflammation. Disease-modifying antirheumatic drugs (DMARDs) prevent joint damage; analgesics reduce symptoms but do not control disease progression. Methotrexate, sulfasalazine, hydroxychloroquine, leflunomide, biologics and targeted synthetic medicines require specialist monitoring.

Medicine	Role	Key monitoring/risk
Methotrexate	Anchor DMARD for inflammatory arthritis	Weekly vs daily dosing error can be fatal; monitor CBC, liver/renal function; infection, pneumonitis and pregnancy risk.
Hydroxychloroquine	DMARD for mild RA/lupus	Retinal toxicity; baseline and ongoing eye screening.
Sulfasalazine	DMARD for peripheral inflammatory arthritis	Rash, blood dyscrasia, liver injury; monitor CBC and liver function.
Leflunomide	Immunomodulatory DMARD	Hepatotoxicity, hypertension, cytopenias and long persistence.
Biologic/targeted medicines	Block cytokines or immune pathways	Serious infection, TB/hepatitis reactivation and vaccination considerations.
Glucocorticoid bridge	Rapid inflammatory suppression while DMARD acts	Hyperglycaemia, infection, osteoporosis and adrenal suppression.

9. Gout: acute flare versus long-term prevention

Gout is caused by monosodium urate crystals. An acute flare is treated with an anti-inflammatory medicine; urate-lowering therapy prevents future flares and joint damage. A hot swollen joint with fever may be septic arthritis, so do not label it gout without appropriate assessment.

Medicine	Acute/long-term role	Safety concerns
NSAID	First-line acute flare if safe	GI bleed, AKI, heart failure, hypertension and anticoagulant interaction.
Colchicine	Acute flare and prophylaxis when starting urate lowering	GI toxicity, marrow suppression, neuromyopathy; dangerous accumulation in renal/hepatic disease and with CYP3A4/P-gp inhibitors.
Oral/intra-articular corticosteroid	Acute flare when NSAID/colchicine unsuitable	Hyperglycaemia, infection risk and joint infection must be excluded before injection.
Allopurinol	Long-term xanthine oxidase inhibition	Rash/SCAR, renal dose adjustment; do not stop/start casually during illness without advice.
Febuxostat	Alternative urate-lowering medicine	Cardiovascular and liver considerations; specialist selection.

10. Osteoporosis and fracture-prevention medicines

Medicine/class	Mechanism/role	Precautions
Calcium/vitamin D	Provide substrate and support mineralisation	Check renal stones, hypercalcaemia and total dietary intake; supplements do not replace antiresorptive therapy when indicated.
Bisphosphonates	Reduce osteoclast bone resorption	Oesophageal irritation, renal impairment, hypocalcaemia and rare jaw/atypical femur problems; take oral dose correctly.
Zoledronic acid	IV bisphosphonate for selected osteoporosis or malignancy	Renal function, hydration, acute-phase reaction and calcium monitoring.
Denosumab	RANKL inhibition reduces osteoclast formation	Hypocalcaemia and rebound vertebral fracture if stopped without follow-on plan.
Teriparatide/abaloparatide	Intermittent PTH-receptor stimulation promotes bone formation	Specialist use; monitor calcium and contraindications.

11. Musculoskeletal red flags and medication limits

Compartment syndrome: escalating pain out of proportion, pain on passive stretch, tense swelling, paraesthesia or weakness. Analgesia must not delay surgical review.
Septic arthritis: hot swollen joint, fever and severe pain with movement. Steroid injection is unsafe until infection is excluded.
Spinal cord/cauda equina compression: new weakness, saddle anaesthesia, urinary retention/incontinence or severe back pain. Urgent imaging and specialist transfer.
Fracture/neurovascular compromise: deformity, absent pulse, cool limb, sensory loss or severe swelling. Immobilise, reassess circulation and transfer.
Rhabdomyolysis: muscle pain/weakness and dark urine after crush injury, seizure or extreme exercise. Renal-protective fluid and electrolyte monitoring are urgent.

12. Clinical scenarios

Scenario 1: Renal/GI risk and fracture pain

An older patient with CKD and previous ulcer has a painful hip fracture. Avoid uncritical NSAID use, support the limb, give protocol-based multimodal analgesia with careful opioid titration and monitor ventilation and BP.

Scenario 2: Septic arthritis versus gout

A hot swollen knee is accompanied by fever and confusion. Do not assume gout or inject steroid. Treat as possible sepsis, obtain urgent aspiration/antibiotic pathway and transfer.

Scenario 3: Compartment syndrome

After a leg fracture, pain is increasing despite opioids and the calf is tense. Reassess pulses, sensation and passive stretch, avoid tight casts/dressings and call for urgent surgical review.

Scenario 4: Colchicine toxicity

A patient with CKD takes extra colchicine and develops vomiting, diarrhoea and weakness. Stop further doses, arrange urgent toxicology/renal assessment and monitor ECG, blood count and organ function.

Scenario 5: Methotrexate dosing error

A patient has taken methotrexate daily instead of weekly and now has mouth ulcers and fever. Treat as a high-risk toxicity, isolate if infection is suspected, avoid further doses and transfer urgently.

Scenario 6: Rhabdomyolysis

After a crush injury, the patient has severe muscle pain and cola-coloured urine. Establish access, monitor ECG/potassium, begin authorised renal-protective fluid and transfer for laboratory and dialysis-capable care.

13. Administration, monitoring and handover

Document pain score and functional impact, injury mechanism, neurovascular status, renal/GI/cardiovascular history, pregnancy possibility, allergies, last analgesic/DMARD dose, medicine concentration, route, exact time, response and adverse effects. Handover red flags, immobilisation, serial circulation checks and need for orthopaedic/rheumatology/renal review.

14. Revision questions

Compare paracetamol, NSAIDs and opioids for acute musculoskeletal pain.
Why can NSAIDs cause AKI and GI bleeding?
What respiratory monitoring is needed after opioid analgesia?
List red flags for compartment syndrome.
Differentiate osteoarthritis and rheumatoid arthritis medicine goals.
Why is methotrexate dosing error dangerous?
What eye monitoring is required with hydroxychloroquine?
Compare acute gout flare treatment with long-term urate lowering.
Why can colchicine become toxic in renal disease?
What are the signs of septic arthritis?
Explain bisphosphonate and denosumab precautions.
What is the risk of abrupt denosumab discontinuation?
List symptoms of spinal cord or cauda equina compression.
How should a fracture with neurovascular compromise be managed?
What are the initial priorities in rhabdomyolysis?
Why should analgesia not be withheld while awaiting diagnosis?
Which patient factors alter NSAID choice?
How should a DMARD toxicity be documented and escalated?

15. Key takeaways

Analgesia is essential, but pain relief must be paired with examination, immobilisation, serial neurovascular checks and red-flag screening.
NSAIDs are effective but can cause GI bleeding, AKI, fluid retention and cardiovascular harm.
Opioids require ventilation monitoring, titration and naloxone/airway preparedness.
A hot swollen joint may be septic arthritis; a severe pain crisis may be compartment syndrome or spinal compression.
DMARDs and bone medicines require long-term laboratory, eye, renal, pregnancy and infection monitoring.
Gout flare therapy and urate-lowering prevention are different clinical decisions.

16. Recommended references for further study

Clinical note: This page supports EMT learning and revision. It does not replace an authorised prescription, local protocol, specialist supervision or patient-specific advice. In a deteriorating patient, stabilise ABCDE, call for advanced help and transfer urgently.

Complete Analgesic Pharmacology Tables

Clinical principle: Assess the cause, intensity, site, quality, duration and functional effect of pain before treatment. Combine non-drug measures with the safest effective medicine, review response, and never allow analgesia to delay urgent diagnosis of shock, acute abdomen, compartment syndrome, meningitis or myocardial infarction. Doses below are common teaching examples; follow the prescriber, Uganda Clinical Guidelines and local protocol.

Analgesic selection and the WHO approach

Use regular non-opioid analgesia for mild pain where appropriate, add an opioid for moderate-to-severe acute or cancer pain, and add an adjuvant when neuropathic, inflammatory or bone pain is present. The modern approach is individualized rather than a rigid ladder: choose the least harmful effective route, schedule background analgesia when pain is continuous, prescribe rescue doses for breakthrough pain, and reassess sedation, respiratory rate, function and adverse effects.

Medicine/class	Pharmacodynamics	Pharmacokinetics	Indications and example adult dose	Contraindications/precautions	Interactions	Common side effects	Serious adverse effects/toxicity	Nursing monitoring and teaching
Paracetamol	Predominantly central analgesic and antipyretic action; little peripheral anti-inflammatory activity.	Rapid oral absorption; hepatic conjugation; a small CYP-mediated fraction forms NAPQI, normally detoxified by glutathione; renal excretion.	Mild–moderate pain/fever. Common adult dose 0.5–1 g orally every 4–6 hours; do not exceed the local maximum, commonly 4 g/day in healthy adults and less in low body weight, malnutrition, liver disease or regular alcohol use.	Severe active liver disease; caution with fasting, malnutrition, alcohol use and duplicate combination products.	Regular prolonged use may increase warfarin effect; enzyme inducers and chronic alcohol exposure may increase toxicity risk.	Nausea, rash; usually well tolerated at therapeutic dose.	Dose-dependent hepatic necrosis, hypoglycaemia, metabolic acidosis and acute kidney injury in severe poisoning.	Count every paracetamol-containing product; record dose/time; monitor liver tests when indicated. Suspected overdose needs urgent level-based assessment and N-acetylcysteine per protocol—do not wait for symptoms.
Ibuprofen / diclofenac (NSAIDs)	Reversible COX inhibition reduces prostaglandin synthesis, producing analgesic, antipyretic and anti-inflammatory effects.	Well absorbed orally, highly protein bound, hepatically metabolized and renally eliminated; effects may outlast plasma half-life.	Inflammatory musculoskeletal pain, dysmenorrhoea, dental/postoperative pain. Ibuprofen commonly 200–400 mg orally every 6–8 hours with food; use the lowest dose for the shortest time. Diclofenac dosing is product/protocol specific.	Active peptic ulcer/GI bleeding, severe renal failure, NSAID hypersensitivity, uncontrolled heart failure; avoid in late pregnancy. Caution in asthma, dehydration, hypertension and older adults.	Anticoagulants/antiplatelets and SSRIs increase bleeding; ACE inhibitor/ARB plus diuretic increases AKI risk; lithium and methotrexate concentrations may rise; avoid combining NSAIDs.	Dyspepsia, nausea, oedema, headache, raised BP.	GI ulcer/haemorrhage, acute kidney injury, bronchospasm/anaphylaxis, myocardial infarction/stroke risk, severe skin reactions.	Check hydration, renal history, BP, ulcer/bleeding risk and pregnancy. Watch urine output, melaena, haematemesis, wheeze and oedema. Give with food if prescribed, but food does not prevent ulceration.
Morphine	Primarily μ-opioid receptor agonism reduces nociceptive transmission and pain perception; also depresses respiratory drive and gut motility.	Variable oral bioavailability from first-pass metabolism; hepatic glucuronidation; active metabolites accumulate in renal impairment.	Severe acute, postoperative, cancer or palliative pain. Dose and route must be individualized and titrated; opioid-naïve adults often start with small immediate-release doses under close observation.	Significant respiratory depression, paralytic ileus; caution in head injury, hypotension, renal impairment, older/frail patients and sleep-disordered breathing.	Benzodiazepines, alcohol, sedating antihistamines, gabapentinoids and other CNS depressants markedly increase sedation/overdose risk; MAOI interactions require specialist advice.	Constipation, nausea, vomiting, pruritus, urinary retention, drowsiness.	Respiratory arrest, profound hypotension, aspiration, dependence and withdrawal.	Before and after dose assess pain, respiratory rate, oxygenation, sedation score, BP and pupils. Hold/escalate for concerning sedation or respiratory depression. Start bowel care when ongoing. Keep naloxone and resuscitation equipment available where required.
Tramadol	Weak μ-opioid agonism plus inhibition of serotonin and noradrenaline reuptake.	Hepatic CYP metabolism to an active metabolite varies genetically; renal elimination; accumulation occurs with renal/hepatic dysfunction.	Selected moderate pain when alternatives are unsuitable; common adult immediate-release dosing is 50–100 mg every 4–6 hours, maximum according to product/local protocol.	Uncontrolled epilepsy, acute intoxication with CNS depressants, severe respiratory depression; caution in older adults and renal/hepatic impairment.	SSRIs/SNRIs/TCAs/MAOIs/linezolid increase serotonin toxicity; medicines lowering seizure threshold increase convulsions; CNS depressants increase overdose risk.	Dizziness, nausea, constipation, sweating, somnolence.	Seizures, serotonin syndrome, respiratory depression, dependence, hypoglycaemia.	Check interacting medicines, seizure history and renal function. Observe mental state, clonus, fever, autonomic instability and respiratory status; teach not to mix with alcohol or unprescribed sedatives.
Codeine	Prodrug partly converted by CYP2D6 to morphine; analgesic effect varies greatly between patients.	Hepatic metabolism; renal elimination. Ultra-rapid metabolizers may develop toxicity while poor metabolizers obtain little benefit.	Short-term selected moderate pain, usually combined with a non-opioid; follow product and age restrictions.	Respiratory depression; breastfeeding; children below locally permitted age and after tonsil/adenoid surgery; caution in renal impairment.	CYP2D6 inhibitors may reduce effect; sedatives/alcohol increase respiratory depression.	Constipation, nausea, drowsiness.	Apnoea, especially in susceptible children or breastfed infants; dependence.	Do not assume predictable effect. Monitor breathing and sedation and avoid duplicate paracetamol in combination tablets.

Adjuvant and specialist analgesics

Medicine	Mechanism/kinetics	Best use and dosing principle	Major cautions/interactions	Adverse effects	Nursing responsibilities
Amitriptyline	Inhibits serotonin/noradrenaline reuptake; anticholinergic and antihistamine effects. Long half-life; hepatic metabolism.	Neuropathic pain; usually started at a low night dose and titrated slowly—not an immediate rescue analgesic.	Recent MI, arrhythmia, severe glaucoma/urinary retention; interacts with MAOIs, serotonergic drugs and CNS depressants.	Dry mouth, constipation, postural hypotension, sedation; overdose may cause seizures and fatal dysrhythmias.	Assess suicide/overdose risk, falls, ECG risk and anticholinergic burden; teach delayed benefit and safe storage.
Gabapentin/pregabalin	Bind α2δ calcium-channel subunit, reducing excitatory neurotransmitter release; not GABA receptor agonists. Renally eliminated unchanged.	Neuropathic pain; titrate gradually and reduce dose in renal impairment.	Respiratory disease, frailty and substance-use risk; additive sedation with opioids/alcohol; do not stop abruptly.	Dizziness, somnolence, ataxia, oedema, weight gain; serious respiratory depression can occur with opioids.	Check eGFR, falls and sedation; counsel on gradual titration/taper and avoiding driving until effects are known.
Ketamine	Non-competitive NMDA antagonism produces dissociative anaesthesia and analgesia while often preserving airway reflexes and sympathetic tone.	Severe acute/trauma pain or procedural sedation by trained teams using weight-based protocol and monitoring.	Severe uncontrolled hypertension, selected psychotic/cardiovascular conditions; additive effects with sedatives.	Emergence reactions, nausea, hypersalivation, hypertension/tachycardia; rare laryngospasm/apnoea.	Use only with airway-skilled staff, oxygen, suction and continuous monitoring; document dissociation, recovery and neurological observations.
Lidocaine topical/local	Blocks voltage-gated sodium channels, preventing nerve impulse conduction; hepatic metabolism.	Local anaesthesia or selected localized neuropathic pain; maximum dose depends on preparation, route and adrenaline content.	Severe conduction disease without pacing, significant hepatic dysfunction; additive toxicity with other local anaesthetics/antiarrhythmics.	Local numbness/irritation; toxicity causes circumoral tingling, tinnitus, seizures, hypotension and ventricular arrhythmias.	Calculate total mg from all sources and patient weight; aspirate/inject incrementally where relevant; stop immediately and activate local-anaesthetic systemic-toxicity protocol if neurological/cardiac signs appear.

Antidotes and urgent toxicity response

Emergency	Key findings	Immediate response	Antidote/specific treatment
Opioid toxicity	Reduced consciousness, slow/shallow breathing, pinpoint pupils may occur, hypoxia.	Call for help, open airway, ventilate with bag-mask and oxygen, monitor ECG/glucose; do not delay ventilation.	Naloxone titrated by the trained prescriber/protocol to adequate ventilation; repeated doses or infusion may be needed because naloxone can wear off before the opioid. Observe for recurrent toxicity and acute withdrawal.
Paracetamol overdose	Early symptoms may be mild despite evolving hepatic injury.	Establish time, formulation, dose and co-ingestants; take paracetamol level at the correct time plus liver/renal tests and INR; contact toxicology service.	N-acetylcysteine according to the treatment nomogram/protocol; start immediately when presentation is late, timing is uncertain or significant toxicity is suspected.
NSAID toxicity/bleeding	Vomiting, epigastric pain, GI bleeding, AKI, acidosis, seizures in severe overdose.	ABC, IV access, renal/electrolyte/acid-base assessment, manage haemorrhage and shock; activated charcoal only when specifically indicated early.	No routine antidote; supportive care, PPI for indicated GI bleeding and specialist management.

Nursing process for a patient receiving analgesics

Assessment: use an age-appropriate pain scale; record pain at rest and movement, likely mechanism, allergies, pregnancy status, renal/hepatic function, ulcer/bleeding risk, medicines, substance-use risk and previous response.
Plan: agree a measurable goal such as ability to breathe deeply, mobilize or sleep—not necessarily zero pain. Match route to urgency and ability to swallow.
Implementation: apply medicine rights, calculate weight-based doses accurately, give at prescribed intervals, combine positioning, splinting, ice/heat where appropriate, relaxation and explanation.
Evaluation: reassess pain and function at the expected onset, and check sedation, respiratory rate, BP, nausea, bowel/bladder function and allergic reactions.
Escalation: urgently report new neurological deficit, pain out of proportion, rigid abdomen, haemodynamic instability, rapidly increasing opioid requirement or inadequate analgesia despite treatment.

High-risk warning: pethidine/meperidine is generally a poor routine choice because its neurotoxic metabolite can accumulate, especially in renal impairment, causing agitation and seizures. Opioids must never be combined casually with benzodiazepines, alcohol or other sedatives.

Revision checkpoints

Distinguish side effects (predictable, often dose-related) from serious adverse effects requiring urgent action.
Know the “triple whammy”: NSAID + ACE inhibitor/ARB + diuretic increases acute kidney injury risk.
For continuous opioid therapy anticipate constipation, nausea and sedation; respiratory depression is an emergency.
Document the pre-dose assessment, exact drug/dose/route/time, response and adverse effects.

Musculoskeletal Medicines: Analgesics, Arthritis, Gout and Bone Safety Read More »

Reproductive System Medicines: Contraception, Obstetric Emergencies and Safety

Why this topic matters in emergency medical care

Reproductive-system medicines influence ovulation, implantation, uterine contraction, cervical ripening, labour, bleeding, infection, lactation and sexual health. In emergencies, EMTs may encounter postpartum haemorrhage, ectopic pregnancy, eclampsia, sepsis, abortion complications, sexual assault or contraceptive adverse effects. The priorities are respectful assessment, privacy, ABCDE stabilisation, pregnancy-aware medication safety and rapid referral.

This lesson is for EMT and nursing education. Follow current Uganda Ministry of Health, WHO, obstetric and facility protocols; do not improvise doses or routes during pregnancy emergencies.

Learning outcomes

Explain the hypothalamic–pituitary–gonadal axis and hormone targets in reproductive pharmacology.
Classify hormonal contraceptives, emergency contraception, uterotonics, tocolytics, fertility medicines, anti-infectives and sexual-health medicines.
Recognise and initially manage postpartum haemorrhage, ectopic pregnancy, eclampsia, sepsis, abortion complications and anaphylaxis to reproductive medicines.
Apply pregnancy, breastfeeding, thrombosis, hypertension, liver disease and drug-interaction precautions.
Provide non-judgemental counselling, protect confidentiality and document medicines and consent accurately.

1. Reproductive physiology and medicine targets

Axis/target	Physiological role	Medicine examples	Emergency relevance
GnRH–FSH/LH axis	Follicle development, ovulation and gonadal hormone production	GnRH analogues, gonadotropins, combined contraceptives	Ovulation medicines can cause ovarian hyperstimulation and ectopic/multiple pregnancy.
Oestrogen/progestin receptors	Cycle control, endometrial stability and pregnancy support	COCs, POPs, implants, injectables, hormone replacement	Oestrogen increases venous thrombosis risk in susceptible patients.
Progesterone receptors	Suppress ovulation, thicken cervical mucus and alter endometrium	Levonorgestrel, medroxyprogesterone, progesterone	Irregular bleeding, mood effects and delayed fertility return with some methods.
Oxytocin receptors	Uterine contraction and milk ejection	Oxytocin, carbetocin	Prevention/treatment of postpartum haemorrhage; water intoxication and uterine hyperstimulation.
Prostaglandin receptors	Cervical ripening, uterine contraction, vasodilation	Misoprostol, dinoprostone, carboprost	Uterotonic effect; fever, diarrhoea, bronchospasm or uterine rupture risk.
Calcium/magnesium neuronal transmission	Neuromuscular excitability and seizure threshold	Magnesium sulfate	Prevention/treatment of eclamptic seizures; toxicity depresses reflexes and breathing.

2. Practical classification of reproductive medicines

Group	Examples	Main role	High-risk concern
Combined hormonal contraceptives	Ethinylestradiol/levonorgestrel and related COCs, patch, ring	Pregnancy prevention and cycle control	Venous thrombosis, stroke, hypertension and smoking-related risk
Progestin-only methods	POP, implant, depot medroxyprogesterone, levonorgestrel IUS	Long-acting or short-acting contraception	Irregular bleeding, injection timing, ectopic pregnancy warning with failure
Emergency contraception	Levonorgestrel, ulipristal, copper IUD	Prevent pregnancy after unprotected sex	Timing, drug interactions, vomiting and need to exclude established pregnancy
Uterotonics	Oxytocin, carbetocin, misoprostol, ergometrine, carboprost	Prevent/treat postpartum haemorrhage, induce labour under protocol	Hypertension, bronchospasm, hyperstimulation and retained placenta
Antihypertensive/eclamptic medicines	Magnesium sulfate, labetalol, hydralazine, nifedipine	Prevent seizures and control severe hypertension	Respiratory depression, hypotension and fetal/maternal monitoring
Anti-infectives	Benzathine penicillin, ceftriaxone, metronidazole, azithromycin	STIs, pelvic infection and obstetric sepsis	Allergy, resistance, pregnancy safety and partner management

3. Combined hormonal contraceptives

Combined oral contraceptives (COCs) contain an oestrogen and a progestin. They prevent ovulation, thicken cervical mucus and alter the endometrium. They are effective when taken consistently but do not protect against STIs; condoms are required for STI prevention.

Benefit	Common effects	Serious warning	Screening point
Reliable reversible contraception	More predictable bleeding, reduced dysmenorrhoea	VTE: unilateral leg swelling, chest pain, sudden dyspnoea	Blood pressure, migraine with aura, smoking/age, VTE history and postpartum status
Cycle suppression	Nausea, breast tenderness, spotting	Stroke or myocardial infarction symptoms	Hypertension, thrombophilia, vascular disease and interacting enzyme inducers
Emergency pill backup	Temporary nausea or bleeding change	Persistent abdominal pain or pregnancy symptoms	Confirm timing, vomiting, drug interactions and pregnancy risk

3.1 When combined methods require caution

Current or previous venous thromboembolism, thrombophilia, stroke, ischaemic heart disease or severe hypertension.
Migraine with aura, heavy smoking at older age, active liver disease or breast cancer.
Early postpartum period, especially when breastfeeding or thrombosis risk is high.
Enzyme-inducing antiseizure medicines, rifampicin/rifabutin and some antiretrovirals can reduce effectiveness.

4. Progestin-only contraception

Method	Medicine/action	Advantages	Emergency/teaching point
Progestin-only pill	Daily progestin suppresses ovulation and thickens mucus	Suitable for many people who cannot use oestrogen	Strict timing varies by product; missed-pill guidance is method-specific.
Implant	Etonogestrel or levonorgestrel release over years	Highly effective, long-acting and reversible	Irregular bleeding is common; pain or infection at insertion site needs review.
Depot injection	Medroxyprogesterone suppresses ovulation for months	Private, effective and less user-dependent	Delayed fertility return, weight/mood changes and bone-density considerations.
Levonorgestrel IUS	Local progestin thickens mucus and thins endometrium	Long-acting, lighter bleeding	Severe pain, fever, heavy bleeding or missing strings may indicate complication.

5. Emergency contraception

Emergency contraception prevents or delays ovulation after unprotected intercourse; it does not terminate an established intrauterine pregnancy. WHO options include levonorgestrel, ulipristal acetate and a copper IUD. A copper IUD inserted within five days is highly effective and provides continuing contraception.

Ask when unprotected sex occurred, current method, last menstrual period, breastfeeding, vomiting and enzyme-inducing medicines.
Exclude symptoms of ectopic pregnancy or established pregnancy; emergency contraception does not treat ectopic pregnancy.
Give the authorised product as soon as possible; ulipristal and levonorgestrel have different interaction and restart rules.
Advise what to do if vomiting occurs, when to test for pregnancy and how to start or resume ongoing contraception.
Provide STI and safeguarding assessment when appropriate, with privacy and consent.

6. Contraceptive interactions and missed doses

Situation	Risk	Response
Enzyme-inducing antiseizure drug	Reduced hormonal contraceptive levels	Use a method unaffected by enzyme induction or specialist guidance; do not rely on guesswork.
Vomiting/diarrhoea after oral dose	Reduced absorption	Follow product-specific missed-dose advice and consider emergency contraception.
Missed COC/POP doses	Ovulation and pregnancy risk	Identify number/timing of missed pills and use the correct protocol.
Ulipristal then immediate hormonal restart	Progestin can reduce ulipristal effect	Follow the recommended delay and barrier method guidance.

7. Uterotonics and postpartum haemorrhage

Postpartum haemorrhage requires simultaneous recognition, uterine assessment, resuscitation, uterine massage, search for trauma/retained tissue/coagulopathy and urgent escalation. A quality-assured uterotonic is used according to the national protocol; medicine choice depends on contraindications and availability.

Medicine	Action	Important contraindication/caution
Oxytocin	Contracts uterine muscle; common first-line uterotonic	Rapid IV bolus can cause hypotension; excessive infusion may cause water intoxication and hyponatraemia.
Carbetocin	Longer-acting oxytocin analogue	Use according to prevention protocol; monitor BP, uterine tone and adverse effects.
Misoprostol	Prostaglandin E1 analogue; uterine contraction and cervical ripening	Fever, shivering, diarrhoea; route and indication are protocol-specific.
Ergometrine/methylergometrine	Powerful sustained uterine contraction	Avoid in hypertension, pre-eclampsia, eclampsia and significant vascular disease.
Carboprost	Prostaglandin F2α analogue for uterine atony	Avoid/caution in asthma; diarrhoea, vomiting and bronchospasm may occur.
Tranexamic acid	Antifibrinolytic stabilises clot	Give early in PPH according to protocol; consider thromboembolic history and renal function.

7.1 EMT response to PPH

Call for help, quantify bleeding where possible and assess airway, breathing, circulation, mental state and shock.
Uterine massage if trained and indicated; inspect for retained placenta/trauma without delaying transfer.
Establish two large-bore IV lines if trained, take blood samples, warm the patient and begin authorised fluid/blood protocol.
Administer the correct uterotonic and early tranexamic acid only under local protocol; check BP/asthma history before ergometrine/carboprost.
Transfer urgently to a facility with obstetric, blood-bank and surgical capability; communicate time, blood loss, tone, placenta status and medicines.

8. Magnesium sulfate and eclampsia

Magnesium sulfate is the medicine of choice in many protocols for preventing and treating eclamptic seizures. It depresses neuromuscular transmission and reduces seizure recurrence. It is not an antihypertensive; severe BP requires a separate authorised medicine and urgent obstetric care.

Check	Before/during magnesium	Toxicity warning
Respiration	Count respiratory rate and assess work of breathing	Respiratory depression or apnoea
Reflexes	Check patellar/deep tendon reflexes when feasible	Absent reflexes may precede severe toxicity
Urine output	Monitor renal function and hourly output in hospital care	Accumulation in oliguria/renal failure
Antidote readiness	Calcium gluconate/chloride protocol and airway support available	Calcium treats toxicity while ventilation and urgent transfer continue

9. Medicines for severe hypertension in pregnancy

Medicine	Role	Safety point
Labetalol	Rapid BP control through alpha/beta blockade	Bradycardia, bronchospasm, heart failure or fetal effects require assessment.
Hydralazine	Direct arteriolar vasodilator	Hypotension, tachycardia and headache; titrate under monitored protocol.
Nifedipine	Calcium-channel blocker for urgent oral BP control	Flushing, headache and hypotension; avoid unsafe rapid-release improvisation.
ACE inhibitors/ARBs	Not for pregnancy hypertension	Fetal renal injury and oligohydramnios risk; check medication history urgently.

10. Fertility medicines and ovarian hyperstimulation

Gonadotropins and ovulation-induction medicines are prescribed in specialist fertility care. Ovarian hyperstimulation syndrome (OHSS) can cause enlarged ovaries, abdominal pain, vomiting, ascites, haemoconcentration, thrombosis and renal injury. Severe breathlessness, reduced urine, sudden abdominal distension or chest pain requires emergency referral.

Ask about recent fertility injections or assisted reproduction in any reproductive-age patient with abdominal pain and vomiting.
Do not assume pelvic pain is gastroenteritis; pregnancy, ectopic pregnancy, torsion and OHSS are time-critical alternatives.
Monitor perfusion, urine output, weight, abdominal girth and respiratory status under specialist care.

11. Reproductive tract infection and STI medicines

STIs require confidential, non-judgemental history-taking, testing, treatment and partner services. Antibiotic selection follows current WHO and national guidance, pregnancy status, allergy and local resistance. Condoms reduce STI transmission; contraception alone does not.

Infection/syndrome	Medicine principles	Safety/teaching
Syphilis	Benzathine penicillin is central to treatment, including pregnancy protocols	Check allergy and observe for reaction; treat partners and prevent congenital infection.
Gonorrhoea	Use current ceftriaxone-based or national regimen	Resistance is increasing; test/treat partners and screen for chlamydia/HIV.
Chlamydia	Doxycycline or azithromycin according to site, pregnancy and guideline	Pregnancy changes choice; partner treatment and abstinence until treated matter.
Trichomoniasis/BV	Metronidazole or alternatives	Alcohol interaction advice and pregnancy/partner guidance are important.
Pelvic inflammatory disease	Broad-spectrum combination treatment	Urgent referral for severe pain, fever, pregnancy, vomiting or tubo-ovarian abscess concern.

12. Medicines in abortion complications and ectopic pregnancy

Misoprostol and mifepristone have specific indications and must be used within authorised, legally compliant services. EMTs should not improvise termination regimens. Heavy bleeding, shock, severe unilateral pain, shoulder-tip pain, syncope or positive pregnancy with abdominal pain may indicate ectopic pregnancy or haemorrhage.

Assess ABCDE, pregnancy possibility, bleeding amount, pain, last menstrual period and previous ectopic/sterilisation.
Keep the patient warm, establish access, monitor and treat shock under protocol.
Do not give oral medicines or food to an unstable patient or delay surgical referral.
Communicate any misoprostol/mifepristone, anticoagulant or herbal medicine exposure confidentially and accurately.

13. Lactation and postpartum medicine safety

Ask whether the patient is breastfeeding before giving sedatives, opioids, antibiotics or hormonal medicines.
Use prescribed compatible medicines where possible; monitor the infant for sedation, poor feeding, diarrhoea or jaundice when risk exists.
Opioids can depress both mother and infant; use the lowest effective prescribed dose and avoid unsupervised combinations.
Postpartum fever, offensive lochia, wound pain, breast infection, severe headache or hypertension require assessment for sepsis or pre-eclampsia.

14. Clinical scenarios

Scenario 1: Postpartum haemorrhage

After delivery, a patient has heavy bleeding and a boggy uterus. Call help, perform ABCDE, massage the uterus if trained, establish access, give protocol uterotonic/tranexamic acid after contraindication checks, resuscitate and transfer urgently.

Scenario 2: Eclampsia

A pregnant patient has a seizure and severe BP. Protect airway and injury, give magnesium sulfate under protocol, treat severe hypertension with an authorised medicine, check glucose and arrange urgent obstetric transfer.

Scenario 3: Ectopic pregnancy

A reproductive-age patient has unilateral abdominal pain, dizziness and light vaginal bleeding. Treat shock, avoid false reassurance, ask pregnancy history and transfer urgently for ectopic assessment.

Scenario 4: Combined contraceptive and thrombosis

A patient using a COC develops sudden dyspnoea and pleuritic chest pain. Consider pulmonary embolism, assess ABCDE and transfer urgently; do not dismiss symptoms as anxiety or a pill side effect.

Scenario 5: Misoprostol exposure with heavy bleeding

A patient reports taking misoprostol and is soaking pads with dizziness. Quantify bleeding, stabilise, protect privacy and refer urgently; do not interrogate or delay care.

Scenario 6: STI with pregnancy

A pregnant patient has pelvic pain, fever and discharge. Treat as possible PID/obstetric infection, use pregnancy-safe protocol and arrange urgent review rather than self-prescribing leftover antibiotics.

15. Documentation, consent and confidentiality

Document pregnancy status, last menstrual period, breastfeeding, method and last contraceptive dose, allergies, sexual-health concerns, medicine name/strength/route/time, bleeding estimate, vital-sign trends, consent and referral. Use private language, avoid judgement, protect records and disclose information only within lawful clinical need.

16. Revision questions

Compare combined and progestin-only contraceptives.
Which contraceptive method also protects against STIs?
What factors reduce emergency contraceptive effectiveness?
List contraindications/cautions for combined hormonal contraception.
Explain the roles of oxytocin, misoprostol, ergometrine and carboprost.
Why is ergometrine avoided in severe hypertension/eclampsia?
What are the signs of postpartum haemorrhage and shock?
What observations are needed during magnesium sulfate therapy?
How is magnesium toxicity managed in principle?
List emergency symptoms of ectopic pregnancy.
Why must STI treatment include partner services and prevention?
What risks should be discussed with breastfeeding patients receiving opioids?
What is OHSS and which signs require urgent referral?
Why should ACE inhibitors/ARBs be reviewed urgently in pregnancy?
How should reproductive emergencies be documented confidentially?

17. Key takeaways

Privacy, consent, pregnancy status and ABCDE assessment are essential in every reproductive emergency.
IM/IV uterotonics, tranexamic acid and resuscitation save lives in postpartum haemorrhage; check contraindications and do not delay transfer.
Magnesium sulfate prevents/treats eclamptic seizures but requires respiratory, reflex and urine monitoring.
Contraception prevents pregnancy but does not protect against STIs except condoms.
Heavy bleeding, shock, ectopic symptoms, sepsis and severe hypertension require urgent referral, not symptom-only treatment.
Use current national/WHO protocols for contraception, STI therapy, pregnancy and breastfeeding.

18. Recommended references for further study

Clinical note: This page supports EMT learning and revision. It does not replace an authorised prescription, local obstetric protocol, senior supervision or patient-specific advice. In a deteriorating patient, stabilise ABCDE, call for advanced help and transfer urgently.

Complete Reproductive-System Pharmacology Tables

Scope: contraceptive choice should be voluntary, confidential and based on pregnancy intention, medical eligibility, effectiveness, side effects, STI protection and access. Obstetric-emergency medicines are given within a resuscitation pathway—never as a substitute for uterine massage, removal of retained tissue, repair of trauma, blood products, seizure/airway care or urgent referral.

Hormonal and emergency contraception

Method/medicine	Pharmacodynamics	Pharmacokinetics	Indication and schedule	Contraindications/precautions	Interactions	Common side effects	Serious adverse effects	Nursing counselling/monitoring
Combined oral contraceptive (ethinylestradiol + progestin)	Suppresses ovulation, thickens cervical mucus and alters endometrium.	Orally absorbed, hepatic metabolism and enterohepatic cycling; daily adherence maintains suppression.	Reversible contraception, cycle control and selected acne/dysmenorrhoea; take one active pill daily according to pack regimen.	Pregnancy, migraine with aura, current/history of VTE or major thrombophilia, severe/uncontrolled hypertension, smoking age ≥35, current breast cancer, severe liver disease; use WHO medical eligibility criteria.	Enzyme inducers such as rifampicin/rifabutin, carbamazepine and phenytoin may reduce efficacy; some antiretroviral interactions require method review.	Nausea, breast tenderness, spotting, mild BP rise, headache.	Venous thromboembolism, stroke, myocardial infarction, severe hypertension.	Measure BP, screen contraindications, explain missed-pill instructions and ACHES warning symptoms; condoms remain necessary for STI protection.
Progestin-only pill	Thickens cervical mucus; suppresses ovulation variably by formulation.	Short duration requires consistent daily dosing; hepatic metabolism.	Contraception when estrogen is unsuitable, including many breastfeeding patients; exact timing window depends on product.	Current breast cancer, severe liver disease; unexplained bleeding needs assessment.	Hepatic enzyme inducers may reduce efficacy.	Irregular bleeding, amenorrhoea, acne, headache.	Rare severe allergy; ovarian cysts/ectopic pregnancy remain diagnostic considerations if pregnancy occurs.	Teach product-specific late/missed-pill action and backup contraception; evaluate persistent heavy bleeding or pregnancy symptoms.
DMPA injection	Long-acting progestin suppresses ovulation and thickens cervical mucus.	Depot release for about 3 months; effects cannot be rapidly reversed and fertility return may be delayed.	150 mg IM every 13 weeks (or product-specific SC regimen) after excluding pregnancy.	Current breast cancer, unexplained bleeding, severe liver disease; consider bone-health and cardiovascular risk.	Few clinically important enzyme-inducer interactions.	Irregular bleeding then amenorrhoea, weight change, headache; delayed fertility return.	Bone mineral density loss during use; rare severe reaction.	Record date/site/lot and next due date; explain bleeding change, delayed fertility return and calcium/vitamin D/weight-bearing health measures.
Etonogestrel/levonorgestrel implant	Continuous progestin suppresses ovulation and thickens mucus.	Slow subdermal release for several years depending on product; hepatic metabolism.	Highly effective long-acting reversible contraception; insertion/removal by trained provider.	Current breast cancer, severe liver disease, unexplained bleeding.	Enzyme inducers may reduce efficacy.	Unpredictable bleeding, headache, acne, breast tenderness.	Insertion-site infection, migration/deep insertion, nerve/vascular injury; ectopic pregnancy is rare but urgent if pregnancy occurs.	Confirm rod palpability, asepsis and documentation; teach wound care, warning signs and that fertility returns quickly after removal.
Levonorgestrel emergency contraception	Delays/inhibits ovulation; does not disrupt an implanted pregnancy.	Rapid oral absorption; hepatic metabolism.	1.5 mg orally once as soon as possible after unprotected intercourse, within the locally recommended window; effectiveness declines with delay.	No restriction based on most chronic disease; assess existing pregnancy and sexual assault needs.	Enzyme inducers can reduce exposure; copper IUD may be preferred when eligible.	Nausea, fatigue, headache, altered next menses.	Rare severe allergy; ectopic pregnancy must be considered with severe pain after a positive pregnancy test.	Repeat dose per product guidance if vomiting soon after; advise pregnancy test if menses is late/abnormal and start ongoing contraception with backup as recommended.
Copper IUD for emergency/ongoing contraception	Copper impairs sperm function and fertilization; local endometrial effect prevents pregnancy.	Local long-term action; no systemic hormone.	Most effective emergency contraception when inserted by a trained clinician within the eligible time window; then provides years of contraception.	Pregnancy, current pelvic infection/purulent cervicitis, unexplained bleeding or distorted uterine cavity; assess post-assault STI risk.	No drug interaction.	Heavier/longer menses and cramps, especially initially.	Perforation, expulsion, pelvic infection around insertion; ectopic pregnancy if method fails.	Aseptic insertion, STI assessment/testing per protocol, teach thread checking and urgent review for pain, fever, discharge, missed period or lost strings.

Postpartum haemorrhage (PPH) medicines

Medicine	Mechanism/kinetics	Use and example dose	Contraindications/interactions	Adverse effects	Nursing/midwifery actions
Oxytocin	Stimulates uterine oxytocin receptors, increasing rhythmic contractions; rapid onset, plasma half-life minutes.	WHO recommends 10 IU IM/IV for PPH prevention after birth. Treatment infusion/bolus regimens are local-protocol specific and require controlled administration.	Caution rapid IV bolus, significant cardiac disease and prolonged high-dose infusion; prostaglandins add uterotonic effect.	Nausea, flushing, hypotension/tachycardia with rapid IV; water intoxication/hyponatraemia with prolonged high dose.	Verify concentration/rate, use pump when available, monitor uterine tone, blood loss, vitals, fluid balance and sodium risk. Maintain cold chain as directed.
Misoprostol	PGE1 analogue increases uterine tone; absorbed orally/sublingually/rectally, hepatic activation.	Prevention where injectable uterotonic is unavailable and treatment adjunct according to WHO/local protocol; dose and route vary by purpose.	Hypersensitivity; do not repeat indiscriminately after an adequate prophylactic dose. Interactions with other uterotonics may intensify effects.	Shivering, fever, diarrhoea, nausea.	Record dose/route/time, distinguish expected fever from sepsis, continue full PPH bundle and referral.
Ergometrine/methylergometrine	Ergot alkaloid causes sustained uterine and vascular smooth-muscle contraction.	Second-line prevention/treatment only when appropriate and per protocol.	Contraindicated in hypertension, pre-eclampsia/eclampsia and significant cardiac disease. CYP3A4 inhibitors raise ergot toxicity.	Nausea, vomiting, hypertension, headache; severe vasospasm, stroke, myocardial ischaemia.	Measure BP before giving; never give when hypertensive; monitor chest pain, neurological signs and uterine response.
Tranexamic acid (TXA)	Antifibrinolytic blocks lysine sites on plasminogen, stabilizing clot; renal elimination.	For clinically diagnosed PPH: 1 g IV over 10 minutes as early as possible and within 3 hours of birth; a second 1 g may be given after 30 minutes if bleeding continues or restarts within 24 hours, following protocol.	Active intravascular clotting, selected thrombotic history; renal dose adjustment. Do not mix through same line with incompatible products.	Nausea, diarrhoea; hypotension if injected too fast; seizures and thrombosis are uncommon.	Time of birth and TXA dose must be documented; infuse over 10 minutes, monitor bleeding/thrombosis/renal function; do not delay surgical/obstetric control.

Hypertensive emergencies and eclampsia

Medicine	Role	Key safety points	Nursing monitoring
Magnesium sulfate	Prevents/treats eclamptic seizures by reducing neuromuscular/CNS excitability; renally eliminated. Loading and maintenance regimens follow local obstetric protocol.	Caution myasthenia gravis, renal failure and heart block; toxicity causes loss of reflexes, respiratory depression and cardiac arrest. Calcium gluconate is the antidote.	Before maintenance dose/infusion check respiratory rate, patellar reflexes, urine output and consciousness; monitor fetal/maternal status. Stop and call urgently for toxicity.
Labetalol	α1 plus β blockade lowers BP; IV or oral use for severe pregnancy hypertension.	Avoid/caution asthma, bradycardia, heart block and heart failure; interacts with other rate-lowering drugs.	Frequent BP/pulse, respiratory assessment, fetal monitoring and watch for hypotension/bradycardia.
Hydralazine	Direct arteriolar vasodilator used IV for acute severe hypertension.	May cause reflex tachycardia, headache and precipitous hypotension; response can be unpredictable.	BP every few minutes during titration, pulse, symptoms, fetal status and fluid balance.
Nifedipine immediate release orally	Dihydropyridine calcium-channel blockade reduces vascular resistance.	Oral protocol option for acute severe hypertension; do not use sublingually. Caution hypotension and concurrent magnesium-related weakness.	Measure BP/pulse at protocol intervals and avoid repeated dosing without documented response.

Safe oxytocic and contraceptive nursing practice

Before contraception: use a pregnancy checklist, BP where estrogen is considered, migraine/VTE/liver/cancer history, medicines, breastfeeding/postpartum status and STI risk; obtain informed choice without coercion.
Before uterotonics: identify the cause of bleeding using the 4 Ts—tone, trauma, tissue and thrombin—while summoning help, massaging the uterus, establishing IV access and quantifying blood loss.
During emergency treatment: monitor airway, oxygenation, BP, pulse, consciousness, uterine tone, ongoing loss, urine output, temperature, clotting and transfusion response.
After stabilization: debrief, document every dose/time/response, check haemoglobin, support breastfeeding where safe, counsel on anaemia treatment and arrange follow-up.

Never combine errors with urgency: oxytocin is measured in international units, magnesium sulfate and TXA in grams, and adrenaline in milligrams/micrograms. Read the ampoule concentration, calculate independently, label syringes/infusions and use a second checker for high-alert medicines.

Reproductive System Medicines: Contraception, Obstetric Emergencies and Safety Read More »

Urinary System Medicines: UTIs, Stones, AKI and Renal Safety

Why this topic matters in emergency medical care

The kidneys regulate fluid, electrolytes, acid–base balance, blood pressure and drug elimination. Urinary medicines can relieve obstruction, treat infection, alter blood pressure, remove fluid, correct electrolyte emergencies or replace renal function. However, the same medicines can worsen acute kidney injury (AKI), accumulate to toxic levels or hide a life-threatening obstructed infection.

This lesson is for EMT and nursing education. Use current Uganda Ministry of Health guidance, local antimicrobial policies, prescriber orders, renal dosing references and age-specific protocols in practice.

Learning outcomes

Explain renal filtration, tubular handling, urine concentration and the renin–angiotensin–aldosterone system.
Classify urinary antimicrobials, diuretics, analgesics for renal colic, alpha blockers, medicines for overactive bladder and renal-protective therapies.
Recognise cystitis, pyelonephritis, urosepsis, obstructed infected kidney, AKI, chronic kidney disease, renal colic and electrolyte emergencies.
Apply safe renal dose and route principles, fluid assessment, urine monitoring and medicine reconciliation.
Identify nephrotoxins, interactions, pregnancy considerations, dialysis issues and escalation triggers.

1. Renal physiology and medicine targets

Each nephron filters plasma at the glomerulus, reabsorbs and secretes solutes through the tubules, and concentrates urine through the loop of Henle and collecting duct. The kidneys activate vitamin D, release erythropoietin and regulate renin. Reduced renal function changes drug clearance, fluid balance, potassium, acid–base status and blood pressure.

Target	Physiological role	Medicine examples	Emergency relevance
Renin–angiotensin–aldosterone system	Maintains vascular tone and sodium retention	ACE inhibitors, ARBs, mineralocorticoid antagonists	Protective in selected CKD but can worsen AKI or hyperkalaemia during dehydration.
Loop sodium–potassium–chloride cotransporter	Concentrates urine and reabsorbs sodium	Furosemide	Rapid diuresis for pulmonary oedema; electrolyte depletion and ototoxicity risk.
Distal sodium–chloride transporter	Regulates sodium and calcium handling	Thiazide diuretics	Hypertension and stone prevention; hyponatraemia, hypokalaemia and hyperglycaemia.
Collecting duct epithelial sodium channel/aldosterone receptor	Sodium retention and potassium excretion	Amiloride, spironolactone	Useful in selected heart failure/aldosterone excess; hyperkalaemia can be fatal.
Vasopressin V2 receptor	Water reabsorption via aquaporins	Desmopressin, vasopressin antagonists	Controls diabetes insipidus or selected hyponatraemia; rapid sodium shifts are dangerous.
Ureteric smooth muscle/alpha-1 receptor	Peristalsis and outlet tone	Tamsulosin and other alpha blockers	May help selected distal stones; dizziness and hypotension risk.

2. Practical classification of urinary medicines

Group	Examples	Main role	Major concern
UTI antibiotics	Nitrofurantoin, trimethoprim, fosfomycin, beta-lactams, fluoroquinolones	Cystitis, pyelonephritis or complicated infection	Resistance, renal dosing, allergy and tissue penetration
Loop diuretics	Furosemide	Oedema, pulmonary oedema, fluid overload	Hypovolaemia, hypokalaemia, hyponatraemia and ototoxicity
Thiazide diuretics	Hydrochlorothiazide, bendroflumethiazide	Hypertension, mild oedema, calcium stone prevention	Hyponatraemia, hypokalaemia, gout and hyperglycaemia
Potassium-sparing/aldosterone blockers	Spironolactone, eplerenone, amiloride	Heart failure, hyperaldosteronism, selected hypertension	Hyperkalaemia and renal accumulation
Renal colic medicines	NSAIDs, paracetamol, opioids	Acute stone pain	NSAID kidney injury/bleeding; opioid sedation and ileus
Alpha blockers	Tamsulosin, doxazosin	Selected distal ureteric stone passage or outlet symptoms	Postural hypotension and syncope
Bladder medicines	Oxybutynin, solifenacin, mirabegron	Overactive bladder	Anticholinergic delirium/retention or hypertension
Electrolyte/acid-base therapy	Calcium, bicarbonate, potassium binders	Selected renal/metabolic emergencies	Arrhythmia, alkalosis and rapid electrolyte shifts

3. Urinary tract infection medicines

UTI treatment depends on site, severity, pregnancy, age, renal function, catheter status and local resistance. Lower UTI (cystitis) usually causes dysuria, frequency and urgency without systemic illness. Pyelonephritis causes fever, flank pain, nausea, vomiting and systemic features. An obstructed infected kidney is a urological emergency requiring drainage as well as antibiotics.

Medicine/group	Typical role	Important safety points
Nitrofurantoin	Lower UTI when renal function and site are appropriate	Does not achieve adequate tissue levels for pyelonephritis; check renal function and pulmonary/hepatic toxicity with prolonged use.
Trimethoprim	Selected uncomplicated lower UTI	Hyperkalaemia, renal impairment, interactions with ACE inhibitors/ARBs/spironolactone and pregnancy considerations.
Fosfomycin	Selected resistant or uncomplicated lower UTI	Use local availability/resistance guidance; not a universal treatment for upper UTI.
Beta-lactams	Selected cystitis or pyelonephritis regimens	Check allergy, renal adjustment and culture results.
Fluoroquinolones	Selected complicated/upper UTI under local specialist guidance	Tendon, neurological, QT and aortic risks; reserve for appropriate indications.
Aminoglycosides	Severe resistant infection in monitored hospital care	Nephrotoxic and ototoxic; therapeutic drug monitoring is essential.

3.1 Antibiotic safety

Obtain urine culture before antibiotics when indicated and when this does not delay treatment in sepsis.
Review previous cultures, recent antibiotics, catheter history, allergies and renal function.
Complete the prescribed course; do not share leftover antibiotics or stop when symptoms first improve.
Escalate for fever with flank pain, rigors, hypotension, vomiting, pregnancy, male UTI, child UTI, catheter-associated infection or immunosuppression.

4. Pyelonephritis, urosepsis and infected obstruction

Pyelonephritis can progress to sepsis, AKI and shock. A ureteric stone or stricture can block infected urine, preventing antibiotics alone from controlling the source. Red flags include severe colic with fever, anuria/oliguria, rigors, hypotension, confusion, rising creatinine or a single functioning kidney.

Perform ABCDE, check glucose, temperature, perfusion, urine output and mental status.
Establish IV/IO access where trained, obtain cultures and lactate when available, and begin sepsis resuscitation under protocol.
Give timely broad-spectrum antibiotics authorised by the local guideline, adjusted for renal function.
Use cautious crystalloid boluses with frequent reassessment, especially in heart or kidney failure.
Arrange urgent imaging and urology review for obstruction; source control may require stent or nephrostomy.

5. Diuretics

Class	Mechanism	Uses	Adverse effects
Loop diuretic	Blocks Na-K-2Cl transport in thick ascending limb	Pulmonary oedema, heart failure, severe oedema	Hypokalaemia, hyponatraemia, hypomagnesaemia, dehydration, hypotension and ototoxicity.
Thiazide	Blocks Na-Cl transport in distal convoluted tubule	Hypertension, mild oedema and selected calcium stones	Hyponatraemia, hypokalaemia, hypercalcaemia, hyperuricaemia and glucose intolerance.
Potassium-sparing	Blocks ENaC or aldosterone receptor	Heart failure, hyperaldosteronism, resistant hypertension	Hyperkalaemia, renal impairment, endocrine adverse effects with spironolactone.
Osmotic	Raises tubular osmotic load	Specialist intracranial-pressure or renal indications	Fluid shifts, pulmonary oedema and electrolyte disturbance.

5.1 Furosemide safety

Assess blood pressure, perfusion, fluid status, lung findings, renal function, electrolytes and recent dose before giving.
In acute pulmonary oedema, nitrates and positive-pressure ventilation may be more immediately important than diuresis.
Rapid IV administration can cause ototoxicity; use the prescribed rate and monitor hearing/neurological symptoms.
Over-diuresis can precipitate AKI, hypotension and electrolyte-driven arrhythmia.

6. Acute kidney injury and nephrotoxic medicines

AKI is a sudden reduction in kidney function, often recognised by rising creatinine or reduced urine output. Causes include dehydration/low perfusion (pre-renal), obstruction (post-renal), infection, toxins, inflammation and intrinsic renal disease. Medicine management requires identifying and stopping avoidable nephrotoxins, correcting perfusion and treating the cause—not simply giving a diuretic.

Nephrotoxin/risk	Potential injury	Safety response
NSAIDs	Reduce renal prostaglandin-mediated perfusion	Avoid in dehydration, shock, CKD or AKI; use safer analgesic plan.
ACE inhibitor/ARB	Reduces intraglomerular pressure; can worsen AKI during hypovolaemia	Medication reconciliation and clinician review during acute illness.
Aminoglycosides/vancomycin	Tubular injury and accumulation	Culture-directed use, renal dosing and drug-level monitoring.
Contrast media	Risk in vulnerable patients	Assess AKI/CKD, dehydration and nephrotoxins; follow imaging protocol.
Herbal/traditional remedies	Unknown nephrotoxic ingredients or contamination	Ask non-judgementally and document all products.

7. Chronic kidney disease and renal dose adjustment

CKD changes clearance, protein binding, acid–base balance, erythropoiesis, bone-mineral metabolism and cardiovascular risk. A “normal” creatinine can be misleading in a small or frail person with low muscle mass. Dose decisions should use the prescribed renal function estimate and specialist guidance.

Renally cleared antibiotics, opioids, gabapentinoids, insulin, anticoagulants and sedatives may need lower doses or longer intervals.
Accumulation can present as confusion, excessive sleepiness, ataxia, respiratory depression, bleeding or severe nausea.
Ask whether the patient receives haemodialysis, peritoneal dialysis or a transplant; timing around dialysis changes medicine removal.
Avoid abrupt fluid loading in anuric patients; pulmonary oedema can develop rapidly.

8. Electrolyte and acid–base emergencies

Emergency	Clinical clues	Medicine/support principle
Hyperkalaemia	Weakness, paraesthesia, bradycardia, peaked T waves, widened QRS	Cardiac monitoring; IV calcium stabilises myocardium, while insulin/glucose and other therapies shift or remove potassium under protocol.
Hypokalaemia	Weakness, cramps, ileus, U waves and arrhythmia	Replace potassium carefully with ECG/renal monitoring; treat magnesium deficiency and cause.
Hyponatraemia	Headache, confusion, seizures, nausea	Identify acute/severe symptoms; hypertonic saline is specialist-controlled because rapid correction can injure the brain.
Metabolic acidosis	Deep breathing, confusion, hypotension	Treat cause such as sepsis, DKA or renal failure; bicarbonate is selective, not routine.
Uraemia	Confusion, pericarditis, pruritus, nausea, bleeding tendency	Urgent renal review; dialysis may be required for refractory complications.

9. Alpha blockers and renal colic

NICE recommends an NSAID as first-line analgesia for suspected renal colic when not contraindicated; IV paracetamol is an alternative when NSAIDs are unsuitable or insufficient, with opioids considered when necessary. Alpha blockers may be considered for selected distal ureteric stones under clinician direction.

Check pregnancy, renal function, GI bleeding, anticoagulants, asthma and allergy before NSAIDs.
Alpha blockers may cause postural hypotension, dizziness and syncope; counsel the patient to rise slowly.
Unrelenting pain, fever, anuria, solitary kidney or rising creatinine requires urgent urological review—not repeated outpatient analgesia.

10. Bladder and urinary-symptom medicines

Class	Examples	Role	Emergency precautions
Antimuscarinics	Oxybutynin, solifenacin, tolterodine	Overactive bladder and urgency	Dry mouth, constipation, blurred vision, delirium and urinary retention; avoid in obstruction or high anticholinergic burden.
β3 agonist	Mirabegron	Relaxes detrusor muscle	May raise BP; review severe hypertension and interactions.
Urinary analgesic	Phenazopyridine where available	Short-term dysuria symptom relief	Does not treat infection; urine discoloration and renal/hepatic cautions.
Desmopressin	V2 agonist reduces urine output	Diabetes insipidus, nocturnal enuresis and selected bleeding disorders	Water intoxication and hyponatraemia; fluid restriction and sodium monitoring matter.

11. Dialysis and medicine considerations

Ask the patient’s dialysis schedule, vascular access type and last session; missed dialysis can cause fluid overload, hyperkalaemia and uraemia.
Never take blood pressure or insert IV lines in a functioning arteriovenous fistula arm unless the renal team authorises it.
Some medicines are removed by dialysis, some are not, and timing may be deliberately post-dialysis.
Patients may be anticoagulated during dialysis; bleeding and access-site complications require careful pressure and documentation.
Urgent transfer is required for pulmonary oedema, severe hyperkalaemia/ECG changes, pericarditis, severe acidosis or altered consciousness.

12. Clinical scenarios

Scenario 1: Pyelonephritis with sepsis

A febrile patient has flank pain, rigors, tachycardia and hypotension. Perform ABCDE, obtain access and cultures where feasible, start authorised sepsis fluids/antibiotics with renal adjustment and transfer urgently. Ask about stones because obstruction changes the required source control.

Scenario 2: Infected obstructed kidney

A patient with renal colic develops fever and anuria. Do not treat as simple pain. Give monitored support, avoid delaying antibiotics and arrange emergency urology assessment for drainage.

Scenario 3: AKI after vomiting

A dehydrated patient has taken ibuprofen and an ACE inhibitor during gastroenteritis. Review nephrotoxins, restore perfusion cautiously, monitor urine output/electrolytes and seek clinician review before further doses.

Scenario 4: Hyperkalaemia

A dialysis patient has weakness and a wide QRS. Place on ECG monitoring, call advanced help and follow the hyperkalaemia protocol. Calcium protects the myocardium but does not remove potassium; insulin/glucose and definitive dialysis may be required.

Scenario 5: Renal colic in pregnancy

A pregnant patient has flank pain and haematuria. Avoid casual NSAID use, assess for infection/obstruction and arrange obstetric/urological advice for analgesia and imaging.

Scenario 6: Diuretic-related collapse

A patient on high-dose furosemide is dizzy with low BP and cramps. Check fluid status, ECG and electrolytes; do not automatically give another diuretic for ankle swelling.

13. Monitoring and documentation

Record urine output, fluid intake/losses, weight when available, BP, pulse, perfusion, lung findings, mental status, medication/last dose, allergy, renal function and ECG. For antibiotics document culture, dose, time and response. For diuretics document urine response and electrolytes. Handover the last dialysis session, access site, obstruction risk and any nephrotoxins.

14. Revision questions

Explain how the kidneys alter medicine clearance.
Differentiate cystitis, pyelonephritis and urosepsis.
Why is an infected obstructed kidney a source-control emergency?
List the common nephrotoxic medicines and risk situations.
Compare loop, thiazide and potassium-sparing diuretics.
What are the danger signs of furosemide over-diuresis?
Why can trimethoprim cause hyperkalaemia?
Explain first-line pharmacological care of renal colic.
When may alpha blockers be considered?
How should dialysis access be protected?
List signs of hyperkalaemia requiring ECG monitoring.
Why is rapid correction of hyponatraemia dangerous?
What are the major cautions for NSAIDs in renal patients?
Compare antimuscarinic bladder medicines with mirabegron.
Which findings suggest AKI?
How does renal failure alter opioid and gabapentinoid safety?
What information is essential in a urinary medicine handover?
Write a safe plan for a patient with UTI, hypotension and reduced urine output.

15. Key takeaways

Renal patients need medicine reconciliation, renal-dose review, electrolyte monitoring and careful fluid assessment.
Fever plus obstruction, anuria or shock is an emergency; antibiotics alone may not control the source.
NSAIDs help renal colic but can worsen AKI, bleeding and heart failure.
Diuretics remove fluid but do not automatically improve kidney function; over-diuresis causes shock and electrolyte arrhythmia.
Hyperkalaemia, severe acidosis, pulmonary oedema and uraemic complications require urgent monitored care and possible dialysis.
Document urine output, last doses, last dialysis, access site, cultures and every medicine/fluid given.

16. Recommended references for further study

Clinical note: This page supports EMT learning and revision. It does not replace an authorised prescription, local emergency protocol, senior supervision or patient-specific advice. In a deteriorating patient, stabilise ABCDE, call for advanced help and transfer urgently.

Complete Urinary and Renal Pharmacology Tables

Dosage and stewardship note: Adult doses below are common teaching examples. Confirm urine culture guidance, pregnancy, allergy, severity, current weight, renal function, obstruction and the Uganda/facility antimicrobial protocol. Adjust renally cleared medicines and never delay drainage or referral when obstruction, sepsis or infected stones are suspected.

Medicines for Urinary Tract Infection

Medicine	Pharmacodynamics and pharmacokinetics	Indications and common adult dosage examples	Contraindications/precautions	Interactions	Side effects and serious adverse effects	Monitoring and nursing responsibilities
Nitrofurantoin	Reduced inside bacteria to reactive intermediates that damage DNA/proteins. Rapid oral absorption and renal secretion produces high urine but poor renal-tissue/serum levels.	Uncomplicated lower UTI when susceptible. Common regimen 100 mg orally twice daily for 5 days, formulation/protocol dependent.	Not for pyelonephritis, prostatitis or urosepsis. Avoid significant renal impairment according to current eGFR threshold; avoid at term pregnancy and in G6PD deficiency where haemolysis risk matters.	Magnesium antacids reduce absorption; probenecid reduces urinary secretion and raises toxicity.	Nausea, headache and brown urine. Serious: pulmonary reaction/fibrosis, hepatitis, neuropathy and haemolysis.	Confirm lower-tract infection and renal function. Give with food. Escalate fever/flank pain/sepsis. Report cough, dyspnoea, jaundice or neuropathy, especially with prolonged use.
Trimethoprim–sulfamethoxazole	Sequentially blocks bacterial folate synthesis; good oral absorption and renal elimination.	Susceptible uncomplicated UTI and selected complicated infections. Double-strength tablet 160/800 mg twice daily; duration commonly 3 days for uncomplicated cystitis and longer for complicated disease, guided by culture/resistance.	Severe sulfonamide allergy, marked liver disease, severe renal failure without monitoring and late pregnancy/young infants. Caution G6PD deficiency and folate deficiency.	Raises warfarin effect, potassium with ACEI/ARB/spironolactone, methotrexate toxicity and sulfonylurea hypoglycaemia.	Rash, nausea and photosensitivity. Serious: Stevens–Johnson syndrome, marrow suppression, hyperkalaemia, AKI/interstitial nephritis and haemolysis.	Culture when indicated; check renal function, potassium, CBC for prolonged therapy and interactions. Stop/escalate rash with mucosal lesions, jaundice or cytopenia signs.
Fosfomycin trometamol	Blocks early peptidoglycan synthesis; single oral dose produces high urine concentrations and is excreted unchanged.	Selected uncomplicated lower UTI: 3 g orally once. Not appropriate for pyelonephritis or sepsis.	Severe renal impairment and complicated upper infection require review.	Metoclopramide can lower urinary concentrations.	Diarrhoea, nausea, headache and vaginitis; rare severe allergy or C. difficile infection.	Dissolve sachet correctly; verify lower UTI and follow culture/local resistance. Reassess non-response or systemic symptoms.
Ciprofloxacin	Fluoroquinolone inhibits DNA gyrase/topoisomerase IV; good oral bioavailability, tissue penetration and renal clearance.	Selected pyelonephritis/complicated UTI when benefits and susceptibility justify use. Common adult example 500 mg orally twice daily for 7 days; regimen varies and resistance may limit use.	Avoid routine uncomplicated cystitis when safer options work. Caution pregnancy, seizure, QT prolongation, aortic disease, myasthenia and renal impairment.	Calcium/iron/antacids reduce absorption; raises theophylline/tizanidine toxicity; QT drugs and warfarin interact.	Nausea and diarrhoea. Serious: tendon rupture, neuropathy, CNS effects, dysglycaemia, QT arrhythmia, aortic events and C. difficile.	Obtain culture for complicated disease. Separate cations. Stop for tendon pain, neuropathy or severe CNS symptoms. Adjust renal dose and reinforce stewardship.
Ceftriaxone	Third-generation cephalosporin inhibits cell-wall synthesis; long half-life permits daily dosing, biliary/renal elimination.	Severe pyelonephritis/urosepsis and initial empiric therapy per local protocol. Common adult 1–2 g IV once daily, severity-dependent.	Severe immediate beta-lactam allergy; hyperbilirubinaemic neonates. Do not mix with calcium-containing IV solutions in neonates.	Warfarin effect may rise; IV calcium compatibility rules.	Diarrhoea, rash and injection pain. Serious: anaphylaxis, C. difficile, biliary sludging and cytopenias.	Obtain cultures before antibiotics when possible without delaying sepsis therapy. Check allergy, observe first doses, review culture for narrowing and monitor response/renal-liver status.

Diuretics and Medicines Affecting Urine Flow

Medicine/class	PD/PK	Indications and dose	Contraindications/interactions	Side/adverse effects	Nursing care
Furosemide	Blocks Na-K-2Cl cotransporter in thick ascending limb, producing potent natriuresis; rapid IV and renal elimination.	Pulmonary/peripheral oedema and selected hyperkalaemia with urine production. Acute adult 20–40 mg IV slowly, higher if chronic exposure/renal dysfunction.	Severe volume/electrolyte depletion and anuria. NSAIDs reduce effect; aminoglycosides increase ototoxicity; digoxin risk rises with low K.	Hypotension, dehydration, low Na/K/Mg, AKI and gout; rapid high dose causes ototoxicity.	Weight, strict balance, BP, oedema/lungs, creatinine and electrolytes. Confirm obstruction is not causing anuria; do not use merely to force urine in established AKI.
Spironolactone	Blocks aldosterone receptor in collecting duct, sparing potassium; hepatic active metabolites.	Ascites, HFrEF, hyperaldosteronism and resistant hypertension. Common 25–100 mg/day depending indication.	Hyperkalaemia, Addison disease and severe renal impairment. ACEI/ARB, trimethoprim and potassium increase hyperkalaemia.	Hyperkalaemia, gynaecomastia, menstrual disturbance; serious arrhythmia.	Baseline/serial K and renal function, BP and weight. Teach avoidance of potassium supplements/salt substitutes unless prescribed.
Mannitol	Filtered but not reabsorbed; increases plasma osmolality and osmotic diuresis.	Selected raised intracranial/intraocular pressure—not routine AKI. Dose is weight-based, commonly 0.25–1 g/kg IV by specialist protocol.	Anuria, pulmonary oedema, severe dehydration and active intracranial bleeding except selected surgery.	Other nephrotoxic agents and diuretics intensify fluid/electrolyte problems.	Initial volume expansion, pulmonary oedema, dehydration, sodium disturbance and AKI.	Use filter set, inspect for crystals, warm/dissolve per product instructions, strict balance, osmolality/electrolytes and respiratory monitoring.
Tamsulosin	Selectively blocks alpha-1A receptors in prostate/ureter, relaxing smooth muscle; hepatic CYP metabolism.	BPH urinary symptoms and selected medical expulsive therapy for ureteric stones. Common 0.4 mg once daily after the same meal.	Severe orthostatic hypotension; caution cataract surgery, hepatic/renal impairment.	PDE5 inhibitors and antihypertensives increase hypotension; strong CYP3A4 inhibitors raise levels.	Dizziness, orthostasis, ejaculatory disorder and headache; rare priapism.	Check lying/standing BP and falls risk. Teach first-dose dizziness and to tell ophthalmic surgeon about current/past use.
Potassium citrate	Alkalinises urine and raises urinary citrate, binding calcium and reducing selected stone formation; renal elimination.	Hypocitraturia, uric-acid and cystine stones under metabolic evaluation. Dose is based on urine citrate/pH, often divided with meals.	Hyperkalaemia, severe renal failure, delayed GI transit and active untreated UTI with urease organisms.	ACEI/ARB/MRA/trimethoprim increase potassium; anticholinergics slow transit.	GI irritation, nausea and hyperkalaemia; serious arrhythmia or GI ulceration.	Monitor K, renal function and urine pH/citrate. Give with food/water, swallow extended-release tablets whole and avoid empiric use without stone evaluation.

Acute Kidney Injury and Electrolyte Emergency Medicines

Medicine	Mechanism	Indication/dose principle	Major risks/interactions	Nursing responsibilities
Calcium gluconate	Stabilises myocardial membrane; does not remove potassium.	Hyperkalaemia with ECG changes: common adult 10 mL of 10% IV slowly, repeat if ECG changes persist.	Extravasation, bradyarrhythmia and digoxin toxicity caution; incompatible with bicarbonate/phosphate in same line.	Continuous ECG, secure IV, confirm concentration and follow with potassium-shifting/removing therapy.
Insulin plus glucose	Insulin activates Na/K ATPase and shifts potassium intracellularly; glucose prevents hypoglycaemia.	Severe hyperkalaemia: common adult 10 units regular insulin IV with 25 g glucose, protocol-dependent; dose reduction may be needed in renal failure/high hypoglycaemia risk.	Severe/prolonged hypoglycaemia and hypokalaemia. Beta-blockers mask symptoms.	Independent dose check, baseline and frequent glucose for at least several hours, repeat potassium/ECG and ensure definitive removal plan.
Nebulised salbutamol	Beta-2 stimulation shifts potassium into cells.	Adjunct in hyperkalaemia; high-dose nebulised regimens are protocol-directed and not monotherapy.	Tachyarrhythmia/ischaemia; beta-blockers reduce response.	Monitor ECG, pulse and potassium; do not rely on it alone.
Sodium bicarbonate	Raises extracellular bicarbonate/pH and may shift potassium when metabolic acidosis is present.	Selected severe metabolic acidosis, sodium-channel blocker toxicity and hyperkalaemia with acidosis. Dose based on blood gas and cause—not routine for every AKI.	Volume/sodium overload, hypocalcaemia, alkalosis and paradoxical intracellular acidosis; incompatible with calcium in same line.	Blood gas, sodium, calcium, fluid status and ventilation; use infusion pump and reassess cause.
Sodium polystyrene sulfonate	GI cation-exchange resin removes potassium slowly.	Selected non-immediate potassium removal; onset is delayed and effect unpredictable. Not emergency monotherapy.	Bowel obstruction/ileus and postoperative bowel; sorbitol increases intestinal necrosis risk.	Constipation, electrolyte disturbance; serious colonic necrosis.	Assess bowel function, avoid when ileus suspected, monitor electrolytes and arrange dialysis when indicated.

Renal Dose Adjustment and Nephrotoxicity

Estimate current renal function: acute creatinine changes make equations unreliable; use trends, urine output and clinical context.
Review high-risk medicines: NSAIDs, aminoglycosides, iodinated contrast, ACEI/ARB during shock/dehydration, metformin during severe AKI/hypoxia, lithium, digoxin, gabapentin and many antimicrobials.
Do not under-treat sepsis: give an appropriate initial antibiotic dose promptly, then adjust maintenance as renal data and drug levels become available.
Dialysis is definitive for selected emergencies: refractory hyperkalaemia/acidosis, severe overload, uraemic complications and dialysable poisoning require urgent referral; medicines must not delay it.

Urinary/Renal Nursing Care Plan

Nursing problem	Outcome	Interventions and rationales	Evaluation
Impaired urinary elimination	Relief of retention/dysuria and measurable output.	Assess bladder, pain, voiding pattern and obstruction; measure output; obtain clean specimen before antibiotics when appropriate; catheterise only when indicated with asepsis.	Improved voiding/output and symptoms.
Risk for electrolyte imbalance	K/Na/acid-base remain within safe range.	Serial electrolytes/ECG, strict balance, medication review, monitor neuromuscular/cardiac signs and escalate thresholds promptly.	Stable rhythm, labs and mental state.
Acute pain from renal colic	Pain controlled without masking sepsis/obstruction.	Assess pain/fever/solitary kidney/anuria, prescribed analgesia/antiemetic, strain urine when ordered, hydrate appropriately but do not force fluids into obstruction.	Pain reduced; red flags referred.
Knowledge deficit	Patient explains medicine course, hydration and return signs.	Teach adherence, culture review, renal dosing, avoidance of OTC NSAIDs/herbals, and urgent return for fever, flank pain, vomiting, anuria or confusion.	Correct teach-back and follow-up.

Authoritative Sources

Urinary System Medicines: UTIs, Stones, AKI and Renal Safety Read More »

Gastrointestinal Medicines: Classes, Emergency Uses and Safety

Why this topic matters in emergency medical care

Gastrointestinal medicines affect hydration, electrolyte balance, bleeding, pain, nausea, bowel motility, infection and nutrition. In the emergency setting, an apparently simple symptom such as vomiting or abdominal pain can represent shock, obstruction, perforation, poisoning, gastrointestinal haemorrhage, pancreatitis or surgical disease. EMTs must know which medicines support physiology, which can mask danger and which require urgent referral.

This lesson is for EMT and nursing education. Always apply current Uganda Ministry of Health guidance, facility protocols, prescriber orders, product information and age-specific algorithms.

Learning outcomes

Describe digestive-system targets including acid secretion, motility, emesis pathways, fluid absorption and intestinal inflammation.
Classify antacids, proton-pump inhibitors, H2 blockers, antiemetics, laxatives, antidiarrhoeals, antispasmodics, pancreatic medicines and selected GI antimicrobials.
Recognise and initially manage dehydration, upper-GI bleeding, acute vomiting, diarrhoea, cholera, constipation, obstruction, pancreatitis and hepatic emergencies.
Select safe routes and monitoring: oral, buccal, rectal, intramuscular, intravenous and nasogastric/enteral routes.
Identify red flags, contraindications, interactions, renal/hepatic dosing issues and when symptom relief must not delay referral.
Calculate, administer, reassess and document GI medicines safely.

1. Digestive physiology and medicine targets

The gastrointestinal tract digests food, absorbs nutrients and water, stores contents and eliminates waste. The stomach secretes acid and intrinsic factor; the pancreas supplies enzymes and bicarbonate; the liver produces bile and metabolises medicines; the intestine controls motility, secretion and absorption. Enteric nerves, serotonin, dopamine, acetylcholine, histamine, prostaglandins and opioid receptors are common pharmacological targets.

Target/pathway	Physiological effect	Medicine examples	Emergency relevance
Gastric proton pump	Final step in acid secretion	Omeprazole, pantoprazole, lansoprazole	Reduces acid injury and supports ulcer therapy; does not replace endoscopy in bleeding.
Histamine H2 receptor	Stimulates acid secretion	Famotidine and related drugs	Acid reduction; dose adjustment may be needed in renal impairment.
Serotonin/dopamine emetic pathways	Nausea and vomiting	Ondansetron, metoclopramide, prochlorperazine	Controls vomiting but can prolong QT, cause dystonia or mask surgical abdomen.
Opioid receptors in bowel	Slow motility and increase sphincter tone	Loperamide, codeine, morphine	Can worsen ileus, toxic megacolon or respiratory depression.
Intestinal chloride/water secretion	Stool fluid and diarrhoea	ORS, zinc, selected antisecretory medicines	Replacement of water and electrolytes is more important than suppressing stool frequency.
Colonic water and motility	Stool formation and defecation	Lactulose, macrogol, senna, bisacodyl	Choice depends on obstruction, hydration, impaction and cause of constipation.
Pancreatic enzymes and bile	Fat and nutrient digestion	Pancreatin, ursodeoxycholic acid in selected disease	Malabsorption and cholestasis need diagnosis rather than empiric emergency dosing.

2. Practical classification of gastrointestinal medicines

Group	Examples	Main role	High-risk concern
Antacids/alginates	Aluminium hydroxide, magnesium hydroxide, calcium carbonate, alginate	Short-term relief of acid symptoms	Electrolyte disturbance, constipation/diarrhoea and drug absorption interactions
Proton-pump inhibitors	Omeprazole, pantoprazole, lansoprazole	GORD, ulcer disease and selected GI bleeding protocols	Long-term nutrient/infection effects and masking of alarm symptoms
H2 blockers	Famotidine	Acid suppression	Renal accumulation and confusion in frail older adults
Antiemetics	Ondansetron, metoclopramide, prochlorperazine, promethazine	Nausea/vomiting from selected causes	QT prolongation, dystonia, sedation and masking of obstruction
ORS/IV fluids	Low-osmolarity ORS, Ringer’s lactate, saline	Dehydration and shock from GI losses	Fluid overload, sodium imbalance and incorrect mixing
Antidiarrhoeals	Loperamide, racecadotril where available	Selected non-bloody diarrhoea	Avoid in dysentery, high fever, ileus or suspected toxic megacolon
Laxatives	Lactulose, macrogol, senna, bisacodyl, glycerol	Constipation and hepatic encephalopathy (lactulose)	Obstruction, dehydration and electrolyte loss
Antispasmodics	Hyoscine butylbromide, dicyclomine	Selected smooth-muscle spasm	Anticholinergic toxicity, glaucoma, urinary retention and masking acute abdomen
GI antimicrobials	Metronidazole, rifaximin and others	Specific diagnosed or suspected infections	Resistance, alcohol interaction, neuropathy and renal/hepatic dosing

3. Antacids, alginates and acid-suppression medicines

Class	Mechanism	Useful role	Safety and interaction points
Antacids	Neutralise existing gastric acid	Rapid short-term dyspepsia relief	Separate from iron, tetracyclines, quinolones and other medicines; aluminium may constipate, magnesium may cause diarrhoea.
Alginates	Form a floating barrier over gastric contents	Reflux symptoms after meals	Check sodium load in heart/kidney failure and use according to product directions.
PPIs	Irreversibly inhibit the gastric H+/K+ ATPase	GORD, peptic ulcer, H. pylori regimens and selected bleeding protocols	Review prolonged use; hypomagnesaemia, B12/iron issues, enteric infection and interactions may occur.
H2 blocker	Blocks histamine-driven acid secretion	Alternative acid suppression	Renal dose adjustment; confusion and bradycardia are uncommon but important.

3.1 Alarm symptoms and GI bleeding

Dysphagia, odynophagia, persistent vomiting, weight loss, anaemia, haematemesis, melaena, palpable mass or progressive symptoms require medical evaluation rather than repeated self-treatment.
In suspected non-variceal upper-GI bleeding, stabilise ABCDE, assess shock, obtain access and arrange urgent endoscopy. Do not allow a PPI dose to delay resuscitation or definitive care.
Ask about NSAIDs, aspirin, anticoagulants, steroids, alcohol, liver disease and previous ulcers.

4. H. pylori and peptic ulcer medicines

H. pylori eradication uses a PPI plus selected antibiotics according to local resistance patterns and previous exposure. The exact regimen is a prescriber decision; incomplete courses increase treatment failure and resistance. Test-of-cure and avoidance of unnecessary NSAIDs are important.

Component	Purpose	Teaching/safety
PPI	Raises gastric pH and supports antibiotic activity	Take as prescribed; may need a washout before some H. pylori tests.
Amoxicillin/metronidazole/clarithromycin or alternative	Eradicates susceptible H. pylori	Check allergy, interactions, pregnancy, QT risk and alcohol with metronidazole.
Bismuth where used	Protective and antimicrobial activity	Dark stools/tongue can occur; salicylate content may matter in bleeding risk.
Sucralfate	Forms a protective barrier over ulcer base	Separate from other medicines; constipation and impaired absorption are possible.

5. Antiemetics

Vomiting may be caused by gastroenteritis, pregnancy, migraine, obstruction, intracranial disease, metabolic disturbance, poisoning or medication adverse effects. Treat the cause and hydration status; antiemetic choice should match the clinical picture.

Medicine/class	Mechanism/role	Major cautions
Ondansetron	5-HT3 receptor antagonist; useful for many acute nausea syndromes	QT prolongation, constipation and headache; correct severe electrolyte disturbance and review interacting QT drugs.
Metoclopramide	Dopamine antagonist with prokinetic action	Dystonia, akathisia, tardive dyskinesia and rare NMS; avoid in obstruction, perforation, GI bleeding or Parkinson disease unless directed.
Prochlorperazine	Dopamine antagonist; antiemetic and vestibular action	Sedation, hypotension, dystonia, QT prolongation and NMS.
Promethazine	H1 antihistamine with anticholinergic/antiemetic effects	Marked sedation, respiratory depression, anticholinergic effects and tissue injury with extravasation.
Domperidone	Peripheral dopamine antagonist in selected settings	QT/arrhythmia risk; contraindications and interactions must be checked.

5.1 Antiemetic safety checklist

Ask whether the patient has severe abdominal pain, distension, no flatus/stool, blood or coffee-ground vomit.
Check pregnancy status, allergies, Parkinson disease, epilepsy, QT-prolonging medicines and renal/hepatic impairment.
Assess hydration, glucose, electrolytes if available and aspiration risk.
Choose the least sedating effective route; do not give oral medicine to a patient with unsafe swallow.
Reassess vomiting, pain, abdominal findings and mental status; symptom relief does not exclude surgical disease.

6. Oral rehydration salts and fluid therapy

Diarrhoeal deaths are usually caused by dehydration and electrolyte loss. WHO recommends low-osmolarity ORS for most diarrhoeal dehydration; the glucose–sodium co-transport system continues to absorb water even during diarrhoea. Continue breastfeeding and age-appropriate feeding when possible. Severe dehydration, shock, altered consciousness or inability to drink requires IV/IO resuscitation and urgent referral.

Clinical state	Management principle	Reassessment
No or mild dehydration	Frequent small sips of correctly mixed ORS, continued feeding and zinc for children according to guideline	Urine output, thirst, mucous membranes, pulse, mental state and stool/vomit losses
Some dehydration	Supervised ORS replacement; use spoon, cup or nasogastric route if safe	Repeat weight or clinical dehydration signs and monitor vomiting.
Severe dehydration or shock	Urgent IV/IO isotonic crystalloid according to age, weight and shock protocol; ORS as soon as safe	Perfusion, capillary refill, BP, pulse, respiratory signs, urine output and electrolytes.
Cholera/profuse watery stool	Rapid ORS/IV replacement, infection prevention, stool surveillance and antibiotics for severe disease per protocol	Frequent fluid balance; losses can become life-threatening within hours.

6.1 Correct ORS preparation

Use the exact packet in the exact volume of safe water stated on the label; too little water can cause dangerous hypernatraemia.
Do not add extra sugar or salt, and do not mix with milk, juice or carbonated drinks unless the product instructions allow it.
Use prepared solution within the manufacturer/WHO recommended time and discard contaminated leftovers.
If the patient vomits, pause briefly and restart with small frequent sips; persistent vomiting requires clinical assessment.

7. Zinc and antidiarrhoeal medicines

Zinc supplementation in children reduces duration and severity of diarrhoeal episodes, but the dose and duration are age-specific. Loperamide reduces intestinal motility and secretion in selected adults with non-bloody diarrhoea; it is not appropriate for every diarrhoeal illness.

Medicine	Appropriate role	Avoid or escalate when
Zinc	Childhood acute diarrhoea according to WHO/UNICEF or national protocol	Check age, formulation and vomiting; continue ORS because zinc does not replace rehydration.
Loperamide	Selected non-bloody diarrhoea in adults	Fever, blood/mucus, suspected invasive infection, ileus, inflammatory bowel flare or young child without specialist direction.
Bismuth subsalicylate	Selected acute diarrhoea or dyspepsia	Salicylate allergy, anticoagulation, active bleeding, renal disease or children with viral illness.
Antibiotics	Specific bacterial dysentery, cholera or other diagnosed indications	Do not use empirically for every watery stool; consider resistance and local guidance.

8. Laxatives and constipation

Class	Examples	Onset/role	Safety points
Bulk-forming	Fibre/ispaghula	Increase stool bulk over days	Require fluid; avoid in obstruction or severe swallowing difficulty.
Osmotic	Lactulose, macrogol, polyethylene glycol	Draw water into bowel; useful for constipation	Bloating, diarrhoea and electrolyte disturbance if excessive; lactulose also treats hepatic encephalopathy.
Stimulant	Senna, bisacodyl	Increase intestinal motility over hours	Cramping and electrolyte loss; do not use repeatedly without diagnosing cause.
Rectal	Glycerol suppository, enema	Local evacuation for distal stool/impaction	Trauma, bleeding, vagal response; avoid with obstruction or recent rectal surgery.
Opioid antagonists	Naloxegol and related specialist medicines	Opioid-induced constipation	May precipitate withdrawal or abdominal pain; specialist selection required.

Red flag: constipation with severe colicky pain, distension, vomiting, fever, peritonism or absent flatus may be obstruction or perforation. Do not repeatedly give laxatives while delaying surgical assessment.

9. Hepatic encephalopathy and lactulose

Lactulose is metabolised by colonic bacteria to acids that trap ammonia and promote its excretion. In hepatic encephalopathy it is titrated to regular soft stools under medical supervision. Excessive diarrhoea causes dehydration, hypokalaemia and worsened confusion. Assess for infection, GI bleeding, constipation, sedatives, electrolyte disturbance and renal failure as triggers.

10. Upper gastrointestinal bleeding

Haematemesis, coffee-ground vomit or melaena may result from peptic ulcer, varices, gastritis, Mallory–Weiss tear, malignancy or anticoagulation. A normal blood pressure does not exclude early shock. Resuscitation and urgent endoscopic assessment take priority over symptom relief.

Assess airway, breathing and circulation; consider aspiration risk and suction. Reduced consciousness with active haematemesis may require advanced airway support.
Place the patient safely, obtain large-bore IV access where trained, monitor ECG/BP/SpO2 and send urgent transfer.
Ask about anticoagulants, antiplatelets, NSAIDs, liver disease, alcohol, previous ulcers and last oral intake.
Use isotonic fluid and blood products according to shock/bleeding protocol; avoid over-resuscitation in portal hypertension or heart failure.
Do not give oral food, drink or tablets to an unstable patient. PPI, vasoactive medicines and antibiotics for variceal bleeding are specialist-directed.
Document estimated blood loss, stool/vomit appearance, vital-sign trends, urine output and every medicine/fluid given.

Possible cause	Clues	Medicine implications
Peptic ulcer/NSAID injury	Epigastric pain, melaena, NSAID use	Stop NSAID pending review; PPI and endoscopy are clinician-directed.
Variceal bleeding	Cirrhosis, massive haematemesis, abdominal distension	Urgent specialist vasoactive drug, antibiotic and endoscopic pathway.
Mallory–Weiss tear	Bleeding after forceful retching	Resuscitate and refer; antiemetic only after obstruction/perforation considered.
Anticoagulant-associated bleed	Warfarin/DOAC/heparin use	Record exact medicine and last dose; reversal requires hospital protocol.

11. Acute abdomen, obstruction and perforation

Antispasmodics and antiemetics may make a patient feel better while a serious surgical condition progresses. Severe or localised pain, guarding, rebound, distension, persistent vomiting, obstipation, fever, shock or pain out of proportion require urgent surgical assessment.

Keep the patient nil by mouth when obstruction or surgical abdomen is suspected.
Give analgesia appropriately; pain relief does not prevent diagnosis when examination and reassessment are documented.
Avoid laxatives and oral medicines in suspected obstruction or perforation.
Monitor for sepsis and dehydration; arrange IV access, fluids and urgent transfer.

12. Pancreatitis and biliary disease

Acute pancreatitis may cause severe epigastric pain radiating to the back, vomiting, ileus, fever and shock. Gallstones and alcohol are common causes, but medicines, hypertriglyceridaemia, trauma and infection are possible. Treatment is supportive: analgesia, carefully monitored fluids, antiemetic therapy and early assessment for organ failure. Avoid NSAIDs when renal perfusion, bleeding risk or dehydration is concerning.

Finding	Concern	EMT action
Persistent vomiting/ileus	Dehydration, aspiration and electrolyte loss	Airway precautions, IV access and antiemetic only after obstruction assessment.
Hypotension/tachycardia	Third-spacing, bleeding or sepsis	Monitored fluid resuscitation and urgent transport.
Jaundice/fever	Cholangitis or biliary obstruction	Sepsis pathway, cultures/antibiotics under protocol and urgent specialist review.
Hypoxia/confusion	Organ failure or aspiration	Oxygen to target, blood gases and advanced support.

13. GI infections and antimicrobial stewardship

Gastroenteritis is often viral or self-limited; antibiotics are reserved for defined indications such as severe cholera, dysentery, selected traveller’s diarrhoea, confirmed pathogens, sepsis or immunocompromised patients according to local guidance. Unnecessary antibiotics cause adverse effects and resistance.

Ask about travel, outbreaks, unsafe water, sick contacts, recent antibiotics, hospital exposure and immunosuppression.
Isolate when infectious diarrhoea is suspected; hand hygiene and safe waste handling protect staff.
Do not use antimotility agents in bloody diarrhoea, high fever, suspected C. difficile or toxic megacolon.
Collect stool or blood specimens when indicated without delaying resuscitation.

14. Special populations

Patient group	Extra risk	Practical implication
Infants/children	Rapid dehydration and weight-based dosing	Use low-osmolarity ORS, zinc and paediatric algorithms; avoid adult antidiarrhoeals.
Pregnancy	Altered motility, aspiration and medicine safety considerations	Check gestational age and use pregnancy-appropriate antiemetic/acid therapy.
Older adults	Polypharmacy, renal impairment, delirium and atypical presentation	Review anticholinergic burden, QT drugs, NSAIDs and dehydration carefully.
Renal disease	Reduced clearance and dangerous electrolyte shifts	Adjust H2 blockers, antibiotics and laxatives; avoid excess magnesium/phosphate.
Liver disease	Bleeding, encephalopathy and altered metabolism	Avoid excess paracetamol/alcohol, monitor sedatives and ask about lactulose adherence.

15. Interactions and medication safety

Combination/situation	Risk	Action
Antacid + tetracycline/quinolone/iron	Reduced absorption through binding or pH change	Separate doses according to product guidance and document the timing.
PPI + selected medicines	Changed absorption/metabolism; long-term nutrient effects	Review ongoing need and interacting drugs; use the lowest effective duration.
Ondansetron + other QT-prolonging drugs	Torsades risk, especially with low potassium/magnesium	Correct electrolytes and obtain ECG in high-risk patients.
Metoclopramide + antipsychotic	Additive dopamine blockade, dystonia or NMS	Avoid duplication and assess Parkinson disease.
Loperamide + opioids	Ileus, constipation and sedation	Do not suppress stool without establishing cause and hydration status.
NSAID + anticoagulant/steroid	GI bleeding and ulcer risk	Ask about all analgesics and seek alternative/gastroprotection guidance.
Lactulose excess	Diarrhoea, hypokalaemia and dehydration	Titrate to the prescribed target and monitor mental status/fluid balance.

16. Clinical scenarios

Scenario 1: Child with diarrhoea

A 2-year-old has frequent watery stools but is alert and able to drink. Start correctly prepared ORS in frequent small amounts, continue feeding/breastfeeding and arrange zinc according to the paediatric protocol. Escalate urgently for lethargy, poor drinking, sunken eyes, weak pulse or reduced urine.

Scenario 2: Suspected cholera

An adult has profuse “rice-water” diarrhoea and weak rapid pulse. Begin rapid ORS/IV rehydration under protocol, apply infection-prevention measures and transfer urgently. Antibiotics may be required for severe disease but must not delay fluids.

Scenario 3: Upper-GI bleed

A patient has melaena, dizziness and a history of ibuprofen use. Keep nil by mouth, assess shock and airway risk, establish monitored access, record anticoagulants/NSAIDs and arrange urgent endoscopy pathway. Do not reassure the patient because the first BP is normal.

Scenario 4: Vomiting with obstruction

A patient has colicky abdominal pain, distension, persistent vomiting and no flatus. Avoid oral medicines, laxatives and large unmonitored fluid loads; protect the airway, establish access and arrange surgical assessment.

Scenario 5: Antiemetic dystonia

A young patient develops neck spasm and upward eye deviation after metoclopramide. Recognise an acute dystonic reaction, protect airway, stop further dopamine-blocking doses and seek protocol-based treatment.

Scenario 6: Hepatic encephalopathy

A cirrhotic patient is confused after constipation. Check glucose, infection, bleeding, sedatives and electrolytes; continue prescribed lactulose plan under clinician direction without causing profuse diarrhoea or dehydration.

17. Calculations and administration checks

For a weight-based medicine, dose = prescribed mg/kg × weight in kg. For liquid preparations, volume = required dose ÷ concentration. For ORS, the packet-to-water ratio must be exact. Check units, concentration, maximum daily dose, renal/hepatic adjustment, route, timing and the last dose already given.

18. Documentation and handover

Document onset and character of pain/vomiting/diarrhoea, stool or vomit appearance, hydration signs, abdominal findings, pregnancy status, allergies, medicine history, suspected trigger, medicine/fluid name and concentration, dose, route, time, response and adverse effects. Handover should state airway risk, haemodynamic trend, fluid losses, urine output and need for surgical, endoscopic or infectious-disease review.

19. Revision questions

Explain why ORS works during diarrhoea.
List signs of severe dehydration and shock.
Why must ORS be mixed with the exact packet volume?
When are zinc and antibiotics used in childhood diarrhoea?
Compare antacids, alginates, PPIs and H2 blockers.
List alarm symptoms in dyspepsia or reflux.
Why should PPI treatment not delay endoscopy in a GI bleed?
Compare ondansetron, metoclopramide and promethazine.
Why can metoclopramide cause dystonia?
When should loperamide be avoided?
List dangerous causes of constipation with vomiting and distension.
Explain lactulose’s role in hepatic encephalopathy.
What are the main causes of upper-GI bleeding?
Why are NSAIDs risky with anticoagulants?
How should a suspected cholera case be managed before transfer?
List medicine interactions that prolong QT.
What are the red flags for acute abdomen or obstruction?
Why are children and older adults high-risk for GI medicine errors?
Which details belong in a GI medicine handover?
Write a safe plan for a patient with persistent vomiting and hypotension.

20. Key takeaways

Hydration, airway protection and diagnosis come before symptom suppression.
Correctly prepared ORS is life-saving for most diarrhoeal dehydration; severe shock needs IV/IO resuscitation.
Antiemetics can cause QT prolongation, dystonia or sedation and may mask obstruction.
GI bleeding, obstruction, perforation and pancreatitis require urgent assessment; do not delay definitive care with oral medicines.
Use antidiarrhoeals and laxatives selectively after excluding infection, obstruction and toxic megacolon.
Always check NSAIDs, anticoagulants, pregnancy, renal/liver disease and recent doses.

21. Recommended references for further study

Complete Gastrointestinal Pharmacology Tables

Safety first: medicine does not replace assessment. Haematemesis, melaena, shock, persistent bilious vomiting, peritonism, severe dehydration, toxic megacolon, jaundice with sepsis, or suspected obstruction requires urgent resuscitation and referral. Doses are common adult teaching examples; use Uganda Clinical Guidelines and local protocols.

Acid suppression, ulcer and reflux medicines

Medicine/class	Pharmacodynamics	Pharmacokinetics	Indications and example dose	Contraindications/precautions	Interactions	Side effects	Serious adverse effects	Nursing monitoring/teaching
Omeprazole (PPI)	Irreversibly inhibits gastric parietal-cell H+/K+-ATPase; suppresses basal and stimulated acid until new pumps form.	Acid-labile; enteric absorbed, hepatically metabolized; short plasma half-life but 24-hour pharmacodynamic effect.	GORD, peptic ulcer, NSAID gastroprotection, H. pylori regimens. Often 20 mg orally once daily 30–60 minutes before food; higher/IV regimens for selected bleeding ulcers are protocol-led.	Alarm symptoms require investigation; caution with severe liver disease and prolonged therapy.	May reduce clopidogrel activation; altered absorption of acid-dependent drugs; high-dose methotrexate interaction; prolonged use may add to hypomagnesaemia risk.	Headache, abdominal pain, nausea, diarrhoea/constipation.	C. difficile infection, severe hypomagnesaemia, interstitial nephritis, B12/iron deficiency and fracture association with long exposure.	Check indication and duration; give before food; review long-term need; monitor magnesium, renal function or nutrition when risk warrants. Do not stop abruptly after prolonged high-dose use without a plan.
Famotidine (H2 blocker)	Competitive H2-receptor blockade reduces acid secretion, especially nocturnal acid.	Good oral absorption; substantial renal elimination; dose reduction may be needed in renal impairment.	Short-term ulcer/reflux treatment when appropriate; dosing depends on indication and renal function.	Caution in renal impairment, older adults and when gastric malignancy has not been excluded.	Fewer CYP interactions than cimetidine; antacids may alter absorption timing.	Headache, dizziness, diarrhoea or constipation.	Confusion, bradyarrhythmia and blood dyscrasias are rare.	Assess symptom response and renal function; investigate dysphagia, weight loss, bleeding or anaemia rather than repeatedly suppressing symptoms.
Antacids	Neutralize existing gastric acid; magnesium salts tend to loosen stools while aluminium/calcium salts may constipate.	Primarily local action; absorbed ions vary and can accumulate in renal failure.	Rapid, short-term dyspepsia relief; dose by product, separate from other medicines.	Severe renal impairment; sodium-containing products in heart failure/hypertension; hypercalcaemia risk with excess calcium.	Reduce absorption of tetracyclines, quinolones, iron, levothyroxine and many others—separate by the recommended interval.	Diarrhoea, constipation, belching.	Electrolyte disturbance, aluminium or magnesium accumulation, milk-alkali syndrome.	Ask about renal/cardiac disease and all medicines; teach that frequent need or alarm symptoms require review.

Antiemetics and prokinetics

Medicine	Mechanism/kinetics	Indications and dosing principle	Contraindications/interactions	Side effects and serious harms	Nursing care
Metoclopramide	D2 antagonism in chemoreceptor trigger zone; 5-HT4 agonism increases upper-GI motility. Renally cleared.	Nausea/vomiting and selected gastroparesis; common adult dose 10 mg up to three times daily for the shortest recommended duration, with renal adjustment.	GI obstruction/perforation/bleeding, Parkinson disease, epilepsy, phaeochromocytoma; avoid with levodopa and other dopamine antagonists.	Drowsiness, diarrhoea; acute dystonia, akathisia, tardive dyskinesia and neuroleptic malignant syndrome.	Use short courses; observe especially children/young adults for oculogyric crisis, neck spasm or restlessness; stop and obtain urgent review for extrapyramidal signs.
Ondansetron	Selective 5-HT3 blockade centrally and on vagal afferents; hepatic metabolism.	Postoperative or chemotherapy-related nausea and selected severe vomiting; dose/route protocol-specific.	Congenital long-QT, significant electrolyte disturbance; contraindicated with apomorphine. Caution with QT-prolonging or serotonergic drugs.	Headache, constipation; QT prolongation/torsades, serotonin toxicity and severe hypersensitivity are uncommon.	Correct potassium/magnesium, consider ECG risk, monitor bowel function and response.
Promethazine	H1 antagonism with anticholinergic/sedative effects; hepatic metabolism.	Nausea, motion sickness or allergic symptoms where appropriate; use the lowest effective dose.	Marked CNS depression, young children under product restrictions; additive sedation with opioids/alcohol.	Dry mouth, blurred vision, urinary retention, drowsiness; severe respiratory depression and tissue injury with improper parenteral administration.	Falls precautions; avoid casual IV use; monitor airway and sedation; warn against driving/alcohol.

Diarrhoea, constipation and inflammatory bowel medicines

Therapy	Pharmacology	Indication/dose	Avoid/cautions	Adverse effects/interactions	Nursing priorities
Low-osmolarity ORS	Glucose-sodium co-transport remains functional in secretory diarrhoea, promoting water and electrolyte absorption.	First-line prevention/treatment of dehydration; give frequent measured amounts according to dehydration plan and replace continuing losses.	Shock, severe dehydration or inability to drink needs urgent IV/NG protocol; incorrect mixing can be dangerous.	Vomiting if given too fast; hypernatraemia/hyponatraemia with wrong dilution.	Mix one packet with the exact clean-water volume printed on it; never add extra sugar/salt; continue breastfeeding/feeding; chart input, stool/vomit losses, weight and urine.
Zinc for childhood diarrhoea	Supports mucosal repair and immune function and reduces duration/severity.	WHO/UNICEF adjunct to ORS: commonly 10 mg daily if under 6 months and 20 mg daily from 6 months for 10–14 days, following local guideline.	Check age/product strength and avoid duplicate supplements.	Nausea/vomiting; quinolones/tetracyclines and iron reduce absorption if given together.	Demonstrate correct dispersible-tablet preparation; emphasize completing the course and continuing ORS.
Loperamide	Peripheral μ-opioid agonist slows intestinal transit and secretion; limited CNS entry at therapeutic dose.	Short-term non-bloody diarrhoea in selected adults only; follow product dose limits.	Children below local age limit, bloody diarrhoea/dysentery, fever with suspected invasive infection, colitis flare or ileus.	Constipation/cramps; overdose or misuse causes fatal QT prolongation and ventricular arrhythmia.	Prioritize rehydration and cause; stop if abdominal distension, constipation or deterioration occurs.
Lactulose	Non-absorbed sugar fermented to osmotic acids; in hepatic encephalopathy traps ammonia as ammonium and increases elimination.	Constipation; hepatic encephalopathy titrated to the prescribed number of soft stools, often 2–3/day.	Obstruction; caution diabetes and electrolyte disturbance.	Flatulence, cramps, diarrhoea, dehydration, hypokalaemia.	Record stool frequency/consistency, mental status, fluid balance and electrolytes; avoid over-treatment.
Bisacodyl	Stimulant laxative increases colonic peristalsis and secretion.	Short-term constipation or bowel preparation; oral or rectal dosing by product/protocol.	Obstruction, acute surgical abdomen, severe dehydration.	Cramps, diarrhoea, electrolyte disturbance; milk/antacids may disrupt enteric coating timing.	Assess cause of constipation; encourage fluid, fibre and mobility when appropriate; avoid habitual unsupervised use.
Mesalazine	Topical colonic anti-inflammatory 5-aminosalicylate action.	Induction/maintenance of mild–moderate ulcerative colitis; formulation and dose depend on disease site.	Salicylate hypersensitivity, significant renal disease.	Headache/GI upset; rare interstitial nephritis, pancreatitis, blood dyscrasia.	Baseline and periodic renal function and blood count; distinguish intolerance from disease flare.

Selected emergency and disease-specific medicines

Situation	Medicine strategy	Critical cautions and nursing action
H. pylori peptic ulcer	Use a locally recommended combination of acid suppression plus two or more antimicrobials for the full course; choice depends on prior macrolide exposure, allergy and local resistance.	Confirm indication, teach exact schedule/adherence, review interactions, and arrange test of cure when recommended. Do not invent a regimen where resistance data and local protocol differ.
Acute upper-GI bleeding	Resuscitation, blood strategy and urgent endoscopy are central. IV PPI is used for selected ulcer bleeding; vasoactive therapy such as octreotide/terlipressin is protocol-led when variceal bleeding is suspected.	Two large-bore IV lines, FBC/coagulation/crossmatch, shock monitoring, NPO, strict fluid balance and early endoscopy/referral. Never let medicines delay haemorrhage control.
Hepatic encephalopathy	Lactulose is titrated to soft stools; rifaximin may be added by specialist protocol.	Search for bleeding, infection, constipation, dehydration, sedatives and electrolyte triggers; protect airway if consciousness falls.
Acute severe nausea/vomiting	Treat cause, replace fluid/electrolytes and select antiemetic by patient risk.	Exclude obstruction, raised intracranial pressure, pregnancy emergencies, DKA and sepsis; monitor QT and sedation risks.

Nursing care plan and patient education

Assessment: abdominal pain pattern, vomiting/stool features, hydration, weight, urine output, pregnancy possibility, medicines including NSAIDs, alcohol, diet, travel/infection exposure and red flags.
Monitoring: vital signs, capillary refill, mental state, mucous membranes, abdominal distension/tenderness, bowel sounds where appropriate, input/output, electrolytes, renal/liver tests and haemoglobin.
Administration: observe NPO status, tube position and swallowing safety; separate interacting antacids; give PPI before food; measure liquid doses accurately.
Education: hand hygiene, safe water/food, ORS mixing, adherence to H. pylori treatment, avoiding unnecessary antibiotics and NSAIDs, and returning immediately for blood in vomit/stool, syncope, persistent vomiting or reduced urine.

Common examination trap: antimotility drugs and routine antibiotics are not the answer to every diarrhoea. Rehydration, continued nutrition, zinc in children and recognition of dysentery, cholera, sepsis or severe dehydration are the priorities.

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