Uncategorized - Nurses Revision

Asthma Emergencies: Assessment, Acute Treatment and EMT Management

Why asthma attacks become emergencies. Asthma is a variable inflammatory airway disease. During an exacerbation, bronchial smooth muscle constricts, airway walls swell and mucus blocks expiratory flow. The patient may deteriorate from a manageable wheeze to exhaustion, silent chest, hypercapnia, respiratory arrest and cardiac arrest. EMTs must assess severity rather than the loudness of wheeze, give bronchodilator and corticosteroid treatment promptly under protocol, identify mimics, monitor response and arrange safe follow-up. Use the current Uganda Clinical Guidelines, facility asthma pathway and the latest GINA recommendations.

1. Learning objectives

Define asthma, exacerbation, status asthmaticus and life-threatening asthma.
Explain airway inflammation, bronchoconstriction, mucus plugging and dynamic hyperinflation.
Perform an immediate ABCDE assessment and classify an attack by clinical severity.
Describe first aid, inhaler/spacer use, nebulised bronchodilators, corticosteroids, oxygen and escalation.
Recognise impending respiratory failure, silent chest, fatigue, altered consciousness and dangerous mimics.
Adapt care for children, pregnancy, older adults and patients with cardiac or other comorbid disease.
Plan observation, discharge, inhaler technique, controller therapy, trigger reduction and a written action plan.

2. What is asthma?

Asthma is a chronic condition with variable respiratory symptoms and variable expiratory airflow limitation. Symptoms include wheeze, breathlessness, chest tightness and cough that change over time and intensity. Triggers may include viral infection, allergens, smoke, air pollution, occupational exposures, exercise, cold air, strong odours, stress and medicines such as aspirin/NSAIDs or beta-blockers in susceptible people.

Concept	Clinical meaning
Bronchoconstriction	Airway smooth muscle narrows the lumen; reliever bronchodilators can reverse this component.
Inflammation and oedema	The airway lining swells and becomes hyper-responsive; inhaled corticosteroids reduce future exacerbation risk.
Mucus plugging	Thick secretions obstruct small airways and may produce a quiet or “silent” chest when airflow becomes critically low.
Exacerbation	An acute or subacute worsening of symptoms and lung function that requires additional treatment.
Status asthmaticus	A severe exacerbation that persists despite initial therapy and needs urgent hospital/critical-care management.

3. Why severe asthma causes respiratory failure

Expiratory airflow becomes limited, so the patient cannot empty the lungs before the next breath. Air trapping and dynamic hyperinflation increase the work of breathing, flatten the diaphragm and reduce venous return. Early in an attack, the patient may hyperventilate and have a low carbon dioxide level. A normal or rising PaCO₂ in a patient who is still struggling is ominous because it suggests fatigue and failing ventilation. Severe hypoxaemia, acidosis, dehydration, mucus plugging and barotrauma can follow.

Increased work: accessory muscle use, prolonged expiration, inability to speak full sentences and exhaustion.
Ventilation mismatch: wheeze, reduced air entry and hypoxaemia from unevenly obstructed airways.
Cardiovascular effects: tachycardia, pulsus paradoxus, hypotension and reduced venous return from hyperinflation.
Terminal signs: confusion, drowsiness, bradycardia, cyanosis, silent chest, poor respiratory effort or arrest.

4. Focused history

Symptoms and time course: onset, speed of worsening, wheeze, cough, chest tightness, nocturnal symptoms, fever, sputum and chest pain.
Previous risk: prior ICU/intubation, hospital admissions, recent emergency visits, previous near-fatal attack, frequent reliever use or poor response to the home plan.
Current treatment: controller inhaler, reliever, adherence, last dose, spacer use, oral steroids, nebuliser access and recent antibiotic/NSAID/beta-blocker exposure.
Trigger and exposure: viral illness, allergen, smoke, occupational dust/chemicals, exercise, cold air, new food/medicine, emotional stress and pregnancy.
Comorbidity/mimics: heart disease, COPD, pneumonia, tuberculosis, anaphylaxis, foreign body, pulmonary embolism, pneumothorax, sickle cell disease and metabolic disease.
Impact: ability to speak, walk, drink, sleep, lie flat and perform usual activities; ask about prior peak-flow values if available.

5. Severity assessment: never grade by wheeze alone

Feature	Mild/moderate	Severe	Life-threatening/impending failure
Speech	Sentences	Words or unable to complete sentences	Unable to speak, drowsy or confused
Position/appearance	Can lie or sit comfortably	Sits upright, anxious, tripod posture	Exhausted, cyanosed, collapsing or reduced consciousness
Respiratory effort	Increased but coordinated	Marked accessory muscle use, fatigue	Silent chest, poor effort, apnoea or paradoxical breathing
Pulse/BP	Tachycardia possible	Marked tachycardia, pulsus paradoxus	Bradycardia, hypotension or peri-arrest signs
SpO₂/PEF	Near usual or mild reduction	Below local target or substantially reduced PEF	Severe hypoxaemia, very low/ unobtainable PEF; use clinical state rather than a number alone
Response	Improves with reliever	Incomplete or short-lived response	No response, rising CO₂, altered mental state

Silent chest is not improvement. A very quiet chest in a struggling patient may mean almost no air is moving. Call senior/critical-care support immediately and prepare assisted ventilation.

6. Differential diagnosis and red flags

Anaphylaxis: wheeze plus urticaria, facial/tongue swelling, stridor, hypotension, vomiting or sudden exposure—give IM adrenaline promptly according to protocol.
Foreign-body obstruction: sudden onset during eating/play, unilateral signs, choking or absent wheeze; use choking algorithm and urgent airway support.
Pneumothorax: sudden pleuritic pain, unilateral absent breath sounds, tracheal deviation, hypotension or severe distress.
Pneumonia/TB: fever, focal crackles, pleuritic pain, haemoptysis, weight loss or exposure; use appropriate infection precautions.
Cardiac failure/pulmonary oedema: orthopnoea, oedema, hypertension, crackles, cardiac history and frothy sputum.
Pulmonary embolism: pleuritic pain, syncope, risk factors, disproportionate tachycardia or hypoxaemia.
Metabolic/toxic causes: diabetic ketoacidosis, salicylate toxicity, panic, severe anaemia or sepsis can mimic breathlessness.

7. First contact and ABCDE actions

Step	Assessment	Immediate action
A – Airway	Speech, stridor, swelling, secretions, ability to protect airway.	Sit upright, suction if needed, treat anaphylaxis/obstruction immediately and call for airway support if consciousness falls.
B – Breathing	Rate, effort, chest movement, wheeze/air entry, SpO₂, speech and fatigue.	Give oxygen to the prescribed target, start inhaled short-acting bronchodilator promptly, reassess continuously and prepare ventilation support.
C – Circulation	Pulse, BP, perfusion, dehydration, arrhythmia and chest pain.	Cardiac monitor, IV access when severe, cautious fluids if dehydrated, treat shock cause and avoid unnecessary delay for tests.
D – Disability	AVPU/GCS, agitation, drowsiness, glucose and ability to cooperate.	Protect from aspiration, check glucose, recognise fatigue and avoid sedatives unless directed for controlled airway management.
E – Exposure	Rash, oedema, fever, trauma, medication patches, trigger and signs of infection.	Remove trigger if safe, maintain warmth/dignity and examine for anaphylaxis, infection or pneumothorax.

8. Immediate treatment of an acute attack

8.1 Position, reassurance and oxygen

Place the patient upright, leaning forward if comfortable; do not force them to lie flat.
Use calm, short explanations. Anxiety increases ventilatory demand, but do not label severe dyspnoea as “just anxiety.”
Give controlled oxygen for hypoxaemia or severe distress, targeting the saturation range in the local protocol. Avoid withholding oxygen from a critically ill patient.
Monitor SpO₂, respiratory rate, pulse, BP, speech, effort and mental status continuously or at very short intervals according to severity.

8.2 Inhaled bronchodilator

Use salbutamol/albuterol by a metered-dose inhaler with spacer for a patient who can cooperate, or a nebuliser for severe distress, poor coordination or inability to use a spacer.
Repeat doses according to the emergency protocol and response. Oxygen-driven nebulisation is preferred for severe hypoxaemia where available.
Add nebulised ipratropium for severe or life-threatening attacks as directed; it can improve bronchodilation when combined with salbutamol.
Check technique: shake inhaler, attach spacer, one puff at a time, slow inhalation and several breaths through the spacer. A mask may be needed for a small child.
Watch for tremor, tachycardia, hypokalaemia, lactic acidosis and arrhythmia, especially after repeated high-dose therapy.

8.3 Corticosteroid early

Systemic corticosteroid reduces airway inflammation and relapse risk; it should be given early in moderate, severe or poorly responsive exacerbations under prescription/protocol. Oral prednisolone is usually effective when the patient can swallow; IV hydrocortisone or another approved preparation is used when vomiting, reduced consciousness or absorption concerns exist. Dose and duration depend on age, weight and the current Uganda/facility guideline.

8.4 Escalation therapies

Urgent senior review for repeated bronchodilator need, persistent hypoxaemia, severe PEF reduction, exhaustion, altered consciousness, silent chest or rising CO₂.
IV magnesium sulfate may be considered for severe, refractory bronchospasm under clinician direction and monitoring.
Prepare non-invasive or invasive ventilatory support when respiratory failure develops. Intubation is high risk because dynamic hyperinflation can cause hypotension and barotrauma.
Use ketamine or other induction/analgesia only by an experienced airway team with full monitoring; do not sedate an unprotected patient merely to make them quiet.
Antibiotics are not routine for an uncomplicated asthma attack; use them only when bacterial infection is clinically suspected or proven.

9. Reassessment after each treatment cycle

Ask whether speech, chest tightness and breathlessness are improving.
Recheck respiratory rate, pulse, BP, SpO₂, air entry, accessory muscle use, mental state and ability to drink.
Repeat PEF/FEV₁ only when the patient can perform it safely; never delay treatment or exhaust a severely breathless patient for a number.
Look for paradoxical deterioration: less wheeze with poorer air entry, rising fatigue, agitation turning to drowsiness, or a normalising/rising CO₂.
Document time, medicine, route, dose, response and escalation. If improvement is incomplete or short-lived, transfer/admit rather than repeatedly discharging.

10. Investigations

Peak expiratory flow: compare with personal best or predicted value when safe; trend is more useful than one isolated reading.
Blood gas: consider in severe or life-threatening disease, exhaustion, altered mental status, hypoxaemia or suspected hypercapnia.
Chest radiograph: not routine for a typical attack; use for focal signs, fever, chest pain, suspected pneumothorax, pneumonia, foreign body or poor response.
ECG/electrolytes: useful with severe tachycardia, repeated beta-agonist doses, chest pain, arrhythmia or cardiac disease.
Blood tests: target them to the clinical question. Eosinophils, infection markers or allergy tests do not replace immediate clinical treatment.
Pregnancy test: consider where imaging or teratogenic medicine decisions may be affected.

11. Severe and life-threatening asthma pathway

Call for help early. Move to a resuscitation area; involve a senior clinician, anaesthesia/critical care and paediatric team where relevant. Continue oxygen, repeated inhaled bronchodilator, ipratropium and systemic corticosteroid under protocol while preparing for ventilatory support.

Use continuous ECG/SpO₂ monitoring and frequent BP/mental-state checks.
Keep the patient upright if conscious; prepare suction, bag-mask, airway adjuncts and a difficult-airway plan.
Do not allow a deteriorating patient to walk to radiology or wait unobserved for a bed.
Secure IV access, take targeted investigations without delaying treatment and maintain careful fluid balance.
Discuss transfer to a facility with mechanical ventilation if the present setting cannot provide it.
After intubation, use a strategy that allows long expiration, low respiratory rate/pressures and permissive hypercapnia under critical-care supervision; squeezing the bag too rapidly can cause auto-PEEP and hypotension.

12. Paediatric asthma emergency care

Assess interaction, feeding, crying/speech, retractions, nasal flaring, respiratory rate, SpO₂, air entry and exhaustion. A child can deteriorate quickly.
Use a spacer with a mask or age-appropriate mouthpiece whenever possible; involve the caregiver and demonstrate technique.
Use weight/age-based salbutamol, ipratropium and steroid regimens from the current paediatric protocol; do not copy adult doses.
Consider bronchiolitis, croup, foreign body, pneumonia, anaphylaxis, congenital heart disease and metabolic illness in a first-ever wheeze.
Admit or refer a child with persistent oxygen need, poor feeding, exhaustion, altered consciousness, previous ICU attack or inadequate home supervision.

13. Pregnancy and comorbidity

Untreated maternal hypoxaemia is dangerous; treat acute asthma promptly and involve obstetric services for severe attacks.
Check medication history, anaemia, cardiac disease, HIV, tuberculosis exposure and sickle cell disease where relevant.
Older adults may have asthma-COPD overlap or heart failure; listen for crackles, assess oedema and review smoking/occupational history.
Diabetes may worsen with systemic steroids; monitor glucose and coordinate adjustment with the clinician.
Do not withhold indicated inhaled corticosteroids or bronchodilators solely because the patient is pregnant; use current specialist guidance.

14. Nursing and EMT care plan

Problem	Interventions	Evaluate
Impaired gas exchange	Upright position, oxygen to target, bronchodilator delivery, airway readiness and continuous SpO₂.	Speech, respiratory effort, SpO₂, air entry, PEF/ABG when appropriate.
Fear/anxiety	Stay with patient, use calm explanations, coach breathing and involve caregiver safely.	Cooperation, reduced distress and ability to use inhaler/spacer.
Medication effects	Check dose/route, monitor pulse, tremor, potassium/glucose and steroid adverse effects.	Clinical response without significant tachyarrhythmia, hypokalaemia or medication error.
Fluid/nutrition risk	Assess hydration, oral intake, IV access and vomiting; avoid unmonitored large fluid loads.	Perfusion, urine output, lung signs and electrolyte/glucose trends.
Knowledge deficit	Teach controller versus reliever, spacer technique, trigger plan and written action plan.	Patient demonstrates technique and explains when to return.

15. Observation, admission and discharge

Consider admission/transfer when

Life-threatening features, persistent hypoxaemia, rising CO₂, poor response or repeated reliever therapy.
Previous ICU/intubation, recent hospitalisation, severe comorbidity, pregnancy, frailty or unreliable access to follow-up.
Need for frequent nebulisers, IV therapy, systemic steroids, ventilatory support or treatment of pneumonia/anaphylaxis.

Before safe discharge

Symptoms and observations are stable after an appropriate observation period and reliever need is decreasing.
Patient can walk, speak and eat/drink without distress; oxygenation is acceptable without new support.
Provide an ICS-containing controller plan when indicated, a reliever plan, correct inhaler/spacer technique and an action plan.
Check adherence, affordability, triggers, smoking exposure, vaccination and follow-up within the recommended interval.
Give written red flags: inability to speak, blue lips, drowsiness, silent chest, worsening despite reliever or need for reliever more often than advised.

16. Long-term prevention of future emergencies

Use an inhaled corticosteroid-containing controller as recommended; reliever-only treatment leaves airway inflammation and exacerbation risk inadequately addressed.
Check technique at every opportunity: device preparation, seal, slow inhalation, breath hold, spacer cleaning and mouth rinsing after steroid inhalation.
Identify and reduce smoke, biomass fuel, occupational dust, mould, allergens, cold air and medication triggers.
Manage rhinitis, reflux, obesity, sleep problems, anxiety, depression and other comorbidity that worsens control.
Encourage vaccination, exercise within control, nutrition, an asthma diary/peak-flow plan and early action at the first deterioration.
Review every exacerbation: Was the trigger recognised? Was the controller used? Was access to medicines interrupted? Is referral needed?

17. Clinical scenarios

Scenario 1 – moderate attack. A 22-year-old is wheezing, speaking in sentences, RR 26/min and SpO₂ 93%. Sit upright, assess ABCDE, give oxygen to the local target, administer salbutamol with spacer/nebuliser, give systemic steroid if indicated, reassess after each cycle and look for infection/anaphylaxis.

Scenario 2 – life-threatening attack. A 45-year-old can speak only single words, has a silent chest, exhaustion and falling consciousness. Activate the emergency team, give oxygen and repeated bronchodilator/ipratropium, administer systemic steroid, obtain access, monitor continuously and prepare expert airway/critical-care support. Do not wait for a routine chest radiograph.

Scenario 3 – child with first wheeze. A 3-year-old has sudden cough and unilateral reduced air entry while eating peanuts. Treat possible foreign-body obstruction; do not repeatedly nebulise and label it asthma. Use the choking/airway pathway and urgent referral.

Scenario 4 – wheeze with shock. A patient develops wheeze, facial swelling and hypotension immediately after an injection. This is anaphylaxis until proven otherwise: give IM adrenaline promptly according to protocol, oxygen, fluids and urgent escalation; bronchodilator is an adjunct, not the first life-saving treatment.

18. Common errors to avoid

Judging severity by wheeze volume rather than speech, effort, air entry, fatigue and mental state.
Delaying bronchodilator or steroid while waiting for PEF, imaging or laboratory results.
Using sedatives, opioids or cough suppressants that depress ventilation in an exhausted patient.
Giving antibiotics for every exacerbation without evidence of bacterial infection.
Forgetting ipratropium, magnesium/critical-care referral or transfer planning in refractory severe disease.
Discharging without checking inhaler technique, controller therapy, access to medication and return precautions.
Ventilating an intubated asthmatic too fast, causing air trapping, hypotension and barotrauma.

ASTHMA emergency check – “BREATHE”
B – Breathing effort, speech and baseline risk
R – Reliever bronchodilator promptly
E – Evaluate oxygenation and dangerous mimics
A – Anti-inflammatory steroid early
T – Trend response, fatigue and mental state
H – Help/critical-care escalation for severe disease
E – Education, action plan and prevention

19. Revision questions

Explain the three main airway changes during an acute asthma attack.
List six findings that indicate severe or life-threatening asthma.
Why can a silent chest be more dangerous than loud wheeze?
Describe the first five minutes of care for a patient with severe asthma.
When are ipratropium, systemic corticosteroids and magnesium considered?
List five differentials for sudden wheeze and one clue for each.
What must be checked before discharging a patient after an exacerbation?
How does an EMT reduce future asthma emergencies through education?

20. Key take-home points

Asthma severity is a clinical judgement; a quiet chest in a tiring patient is an emergency.
Position upright, assess ABCDE, provide oxygen when indicated and deliver inhaled bronchodilator without delay.
Systemic corticosteroids should be given early in moderate/severe exacerbations under protocol.
Look actively for anaphylaxis, foreign body, pneumothorax, pneumonia, cardiac disease and pulmonary embolism.
Repeated reassessment and early critical-care referral save lives; treatment response must be documented.
Controller therapy, inhaler technique and a written action plan prevent future attacks.

Safety note: This is educational content for EMT students, not a prescription. Exact inhaler/nebuliser doses, oxygen targets, steroid regimen, magnesium use, paediatric schedules and ventilator settings must follow the current Uganda Ministry of Health/facility protocol and senior clinical supervision.

References for further study

Global Initiative for Asthma (GINA): current strategy and summary guides
WHO: Asthma fact sheet
NHS: Asthma and hospital treatment of attacks
Uganda Ministry of Health: current asthma, emergency-care and essential-medicines guidelines.

Asthma Emergencies: Assessment, Acute Treatment and EMT Management Read More »

Cholera in Emergency Care: Rehydration, Shock and Outbreak Management

Why every EMT must recognise cholera early. Cholera is an acute intestinal infection caused by toxigenic Vibrio cholerae, usually acquired through contaminated water or food. Profuse watery diarrhoea and vomiting can remove litres of fluid and electrolytes in a few hours. Death is preventable when dehydration is assessed quickly, oral or intravenous rehydration starts immediately, antibiotics are used selectively, and transmission is interrupted. This lesson follows emergency principles; always check the current Uganda Ministry of Health cholera guideline, local case definition, treatment-centre protocol, antimicrobial susceptibility advice and referral pathway.

1. Learning objectives

Explain the organism, transmission cycle, incubation and pathophysiology of cholera.
Recognise suspected cholera and distinguish no, some and severe dehydration.
Perform safe triage and ABCDE assessment while beginning rehydration without delay.
Describe oral rehydration, intravenous fluid resuscitation, ongoing replacement, nutrition and monitoring.
Explain when antibiotics, zinc and other supportive treatments are appropriate—and what to avoid.
Apply isolation, PPE, environmental cleaning, safe specimen collection and waste management in a cholera treatment area.
Plan discharge teaching, notification, outbreak control, WASH interventions and oral cholera vaccination.

2. Definition and cause

Cholera is an acute secretory diarrhoeal illness caused by toxigenic strains of Vibrio cholerae, most importantly serogroups O1 and O139. The organism colonises the small intestine and produces cholera toxin. The toxin drives chloride and water secretion into the intestinal lumen without causing the invasive bloody inflammation typical of dysentery. Many infections are asymptomatic or mild, but severe dehydration can cause hypovolaemic shock, acute kidney injury, arrhythmia and death.

Term	Emergency meaning
Suspected cholera	Acute watery diarrhoea, often with vomiting, in a person from an outbreak/affected area or with an epidemiological link; use the current national case definition.
Rice-water stool	Pale, cloudy watery stool with flecks of mucus; it is suggestive but not required for diagnosis.
Acute watery diarrhoea	Three or more unusually loose/watery stools within 24 hours; assess every patient for dehydration and dangerous causes.
Severe dehydration	A life-threatening deficit of water and electrolytes causing shock, altered consciousness, anuria/oliguria or marked clinical signs.
Cholera treatment centre (CTC)	A designated area that separates patient flow, provides rapid rehydration, infection prevention, surveillance, laboratory referral and safe sanitation.

3. Transmission and risk factors

Faecal–oral transmission occurs when contaminated water, food, hands, utensils or surfaces reach the mouth.
Risk increases where water treatment, latrines, handwashing, food safety and waste disposal are disrupted by flooding, displacement, conflict or overcrowding.
Eating raw seafood or food handled by an infected person can transmit disease; cooked food can become contaminated after cooking.
Household contacts, healthcare workers and caregivers are exposed during cleaning, toileting, handling vomit/stool and laundering.
Vibrio can survive in aquatic environments; epidemics require both clinical care and community WASH control.
Incubation is commonly short—hours to several days—so ask about recent water, food, travel, community cases and household illness.

Important: Cholera is not spread by casual proximity alone. The greatest risk comes from ingestion of contaminated material. Good hand hygiene, safe water, dedicated toilets and correct cleaning protect both patients and staff.

4. Pathophysiology and why shock develops

Cholera toxin activates adenylate cyclase in intestinal epithelial cells, increasing cyclic AMP and opening chloride channels. Sodium, bicarbonate, potassium and large volumes of water follow into the bowel. The patient loses extracellular fluid rapidly, causing intravascular depletion, metabolic acidosis, hypokalaemia and prerenal kidney injury. Vomiting adds further losses. The abdomen may remain soft and non-tender despite severe illness, so the stool volume and perfusion signs matter more than abdominal pain.

Early compensation: thirst, tachycardia, dry mouth and reduced urine while blood pressure may remain normal.
Progressive dehydration: sunken eyes, poor skin turgor, weak pulse, postural dizziness, lethargy and delayed capillary refill.
Shock: hypotension, cold/mottled skin, altered consciousness, very weak or absent peripheral pulse, anuria and collapse.
Electrolyte complications: cramps, weakness, ileus, arrhythmia, seizures and worsening acidosis.
Rehydration risk: over-rapid or unmonitored fluid can cause pulmonary oedema, especially in infants, older adults, pregnancy or heart/renal disease.

5. Clinical features

Stage/pattern	Possible findings	EMT priority
Early or mild	Watery diarrhoea, thirst, nausea, mild weakness, normal mentation and preserved urine.	Start ORS, count stools, identify risk, educate and monitor for progression.
Some dehydration	Restlessness, irritability, dry mouth, sunken eyes, reduced tears, fast pulse, decreased urine, skin pinch slow to return.	Supervised oral rehydration, repeat assessment and referral if unable to drink or losses continue.
Severe dehydration/shock	Lethargy/unconsciousness, very weak pulse, hypotension, cold skin, minimal urine, markedly delayed capillary refill, deep breathing.	Resuscitation area, IV/IO access if trained, immediate IV rehydration, oxygen if indicated and senior review.
Complicated disease	Persistent vomiting, severe cramps, hypoglycaemia, renal failure, altered consciousness, seizures, pulmonary oedema or suspected sepsis.	Continuous monitoring, laboratory assessment, critical-care/medical referral and correction of the complication.

6. Triage and infection-control precautions at first contact

Ask about watery diarrhoea and vomiting before the patient enters a crowded waiting area; provide a nearby toilet or stool container.
Perform hand hygiene and wear gloves. Add apron/gown, mask and eye protection when splash from vomit or stool is possible.
Place suspected cases in the designated cholera/acute-diarrhoea area with a clear one-way flow for patients, staff, specimens and waste.
Immediately identify shock, altered consciousness, severe dehydration, inability to drink, pregnancy, infancy, older age, malnutrition and serious comorbidity.
Begin ORS while waiting for assessment in any alert patient who can drink; do not make a dehydrated patient wait for a stool result.
Notify the responsible clinician, infection-control lead and public-health surveillance team according to local policy.

7. Focused history and examination

History

Time of onset, number/volume of stools, vomiting frequency, thirst, dizziness, cramps and last urine.
Ability to drink, breastfeed or retain ORS; recent oral medicines and fluid already taken.
Household, school, workplace or camp cases; water source; food eaten; sanitation and recent travel/movement.
Age, weight, pregnancy, breastfeeding, diabetes, renal/heart disease, HIV/immunosuppression, malnutrition and recent antibiotics.
Blood in stool, severe abdominal pain, high fever, rash, altered consciousness or focal symptoms suggesting another diagnosis.

Examination

General appearance, mental state, ability to sit/stand and severity of thirst.
Pulse rate/quality, blood pressure, capillary refill, skin temperature/colour and respiratory pattern.
Eyes, mucous membranes, tears in children, skin pinch, extremity temperature and urine output.
Weight when possible—use the pre-illness weight if known to estimate the fluid deficit.
Abdomen for distension, tenderness, ileus or an alternative surgical diagnosis; inspect stool only with appropriate PPE.

8. ABCDE emergency assessment

Step	Assessment	Immediate action
A – Airway	Vomiting, reduced consciousness, aspiration risk and secretions.	Position safely, suction if trained, protect airway and keep an emesis container available.
B – Breathing	Rate, depth, SpO₂, work of breathing and acidotic deep respirations.	Give oxygen for hypoxaemia or shock according to protocol; reassess after fluids and prevent aspiration.
C – Circulation	Pulse, BP, capillary refill, skin, dehydration signs, stool/vomit volume and urine.	Start ORS or IV crystalloid immediately. Establish IV/IO access if trained and prepare rapid transport for shock.
D – Disability	AVPU/GCS, glucose, cramps, weakness and seizures.	Check glucose, treat hypoglycaemia/seizures under protocol and investigate severe electrolyte disturbance.
E – Exposure	Temperature, stool appearance, abdominal signs, rash, pregnancy and comorbidities.	Maintain dignity and warmth, collect safe specimen if indicated and place in appropriate isolation flow.

9. Assessing dehydration

Feature	No dehydration	Some dehydration	Severe dehydration
Behaviour	Alert, normal activity	Restless/irritable, weak	Lethargic, floppy or unconscious
Eyes/mouth	Normal	Sunken eyes, dry mouth, reduced tears	Very sunken eyes, extremely dry mucosa
Thirst/drinking	Drinks normally	Thirsty, drinks eagerly	Unable to drink or drinks poorly
Pulse/perfusion	Normal, warm peripheries	Fast pulse, delayed refill	Very weak/absent pulse, cold mottled skin, prolonged refill
Skin pinch	Returns immediately	Returns slowly	Returns very slowly
Urine	Normal	Reduced	Minimal or absent
Management direction	ORS after each stool, advice and safety net	Supervised oral rehydration and repeat examination	Immediate IV/IO rehydration, close monitoring and senior/critical-care referral

Do not use one sign in isolation. Infants, severely malnourished people, older adults, pregnant patients and people with chronic disease may show atypical signs. Use trends, urine output, mental state and perfusion together.

10. Rehydration: the life-saving treatment

10.1 Oral rehydration solution (ORS)

Give standard low-osmolarity ORS made with the correct amount of safe water. Use the packet instructions; an overly concentrated solution can worsen hypernatraemia.
For an alert patient with no severe dehydration, give frequent small sips with a cup or spoon. After each stool, continue age/weight-appropriate replacement and replace vomited fluid.
If vomiting occurs, pause briefly and restart more slowly. Persistent vomiting, inability to drink or worsening perfusion requires IV assessment.
Continue breastfeeding and age-appropriate feeding. ORS replaces water and salts but does not replace nutrition.
Never mix ORS with milk, juice, soda or unsafe water; discard prepared solution according to local guidance.

10.2 Supervised oral rehydration for some dehydration

Under the current national protocol, give a measured weight-based volume of ORS over the first few hours (commonly 75 mL/kg over 4 hours for children), reassessing pulse, mental status, thirst, tears, skin signs and urine. Continue replacing ongoing losses and refer for IV therapy if the patient deteriorates, cannot drink or fails to improve.

10.3 Intravenous rehydration for severe dehydration or shock

Move to a resuscitation area, call a senior clinician, monitor continuously and obtain weight if this will not delay treatment.
Use Ringer's lactate where recommended; normal saline may be an alternative if Ringer's lactate is unavailable. Avoid hypotonic fluids for shock.
Use the current weight-based Plan C schedule. A commonly taught WHO schedule is 100 mL/kg total: 30 mL/kg rapidly then 70 mL/kg over the next period, with the timing adjusted for infants versus older children/adults. Follow the Uganda protocol and reassess after each phase.
Begin ORS as soon as the patient can drink; give through a cup, nasogastric tube or other approved route under supervision if safe.
Reassess pulse, blood pressure, capillary refill, mental state, breathing, lung sounds and urine at frequent intervals. Stop or slow fluids and seek senior review for crackles, worsening hypoxaemia or pulmonary oedema.
In severe malnutrition, heart failure, renal failure, pregnancy or paediatric shock, use the specific protocol and senior supervision rather than copying an adult schedule.

11. Replace ongoing losses and correct complications

Measure or estimate every stool and vomit; use a stool chart and weigh diapers/containers where feasible.
Continue ORS after each watery stool and adjust IV replacement to clinical response and facility protocol.
Check electrolytes, glucose, renal function and acid–base status in severe disease or prolonged losses; correct potassium and glucose carefully.
Treat hypoglycaemia promptly. Severe cramps, weakness, arrhythmia, seizures or ileus may signal electrolyte disturbance.
Do not routinely give antidiarrhoeal antimotility agents, opioids or unnecessary antiemetics; they can mask deterioration or cause adverse effects. Use prescribed medicines only when clinically indicated.
Continue nutrition and breastfeeding. In children with acute diarrhoea, provide zinc according to the national paediatric protocol.

12. Antibiotics and other medicines

Rehydration is the cornerstone. Antibiotics are an adjunct, not a replacement for fluid and electrolyte treatment. They may be recommended for severely ill patients, very high-output disease or selected high-risk cases according to current Uganda guidance and local susceptibility patterns.

Collect a stool specimen when indicated and do not delay resuscitation while waiting for culture.
The prescriber should choose an effective local agent, route, dose and duration after considering age, pregnancy, allergy, renal/liver function and recent antibiotic exposure.
Use susceptibility results and outbreak guidance to avoid ineffective therapy and prevent AMR.
Document indication, time, medicine, route, response and adverse effects; review whether therapy can be stopped or narrowed.
Avoid routine prophylactic antibiotics for every contact and avoid self-medication or leftover drugs.

Exam principle: A patient in cholera shock dies from dehydration, not from lack of an antibiotic. Start the right fluid immediately, then use antibiotics selectively.

13. Investigations and diagnosis

Diagnosis during an outbreak is primarily clinical and epidemiological; laboratory confirmation supports surveillance and guides public-health action.
Collect stool or rectal-swab specimens using the approved container, label at bedside, maintain the cold chain and notify the laboratory before transport.
Do not delay ORS, IV fluids, referral or isolation while waiting for culture or molecular testing.
In severe disease, monitor full blood count, electrolytes, urea/creatinine, glucose, lactate and blood gas when available.
Consider malaria, dysentery, typhoid, acute gastroenteritis, food poisoning, rotavirus/norovirus, diabetic ketoacidosis, bowel obstruction, appendicitis and toxic ingestion when the presentation is atypical.
Blood in stool, high persistent fever, severe focal pain, peritonism or no improvement should prompt evaluation for another or additional diagnosis.

14. Cholera treatment-centre nursing care

Care domain	Detailed nursing/EMT actions	Escalation signs
Fluid balance	Record intake, ORS, IV fluid, stool/vomit output, urine, weight and time of each reassessment.	Persistent shock, no urine, rising losses, sudden weight change or fluid overload.
Perfusion	Trend pulse, BP, capillary refill, skin temperature/colour and mental status; keep the patient warm.	Weakening pulse, hypotension, mottling, confusion, collapse.
Airway/aspiration	Position safely, keep suction available, observe vomiting and protect a drowsy patient.	Reduced consciousness, recurrent aspiration, cyanosis or respiratory distress.
Skin and dignity	Clean and dry the perineum, use barrier protection, change linen, prevent pressure injury and provide privacy.	Excoriation, pressure injury, inability to care for self.
Medication safety	Check allergies, weight, renal function, dilution, time and response; document antibiotics and zinc when prescribed.	Rash, wheeze, arrhythmia, worsening renal function or medication error.
IPC and waste	Hand hygiene, PPE, dedicated equipment, safe stool/vomit disposal, chlorine/environmental cleaning and safe laundry.	Spill, staff exposure, cross-contamination or inadequate isolation capacity.

15. Infection prevention in the health facility

Use a dedicated cholera area with separate entry, triage, rehydration, observation, admission, discharge, toilet and waste routes.
Perform hand hygiene with soap and safe water; alcohol rub may not replace washing when hands are visibly soiled.
Wear gloves and apron/gown for patient or excreta contact; add eye/face protection for splash risk. Remove PPE safely and clean hands immediately.
Use dedicated thermometers, weighing scales and stethoscopes where possible; clean and disinfect shared equipment between patients.
Disinfect high-touch surfaces, beds, toilets, buckets and spills with the locally approved chlorine concentration and contact time.
Handle linen, stool containers, vomit and dead bodies as infectious material; follow facility waste and burial policy.
Protect food handlers and cleaners, provide staff training, monitor exposures and report occupational incidents promptly.

16. Discharge and follow-up teaching

Explain how to mix ORS with safe water, how often to sip it and how to replace every continuing watery stool.
Teach caregivers to continue breastfeeding and feeding, wash hands after toileting/cleaning and before preparing food, and use a safe latrine.
Provide clear return precautions: increasing thirst, inability to drink, repeated vomiting, little/no urine, fainting, confusion, blood in stool, fever, severe abdominal pain or worsening weakness.
Advise safe water treatment, covered storage, food cooking/reheating, safe disposal of child faeces and cleaning of contaminated surfaces.
Notify the surveillance team and link households to community health workers for contact advice and WASH support.

17. Community outbreak response

Report suspected cases through the established public-health channel; use a line list with onset, location, exposure, treatment and outcome.
Open oral rehydration points and treatment centres close to affected communities while maintaining safe patient flow.
Provide safe water, chlorine/household water-treatment advice, handwashing stations, latrines and hygiene education.
Investigate water sources and food chains, communicate risk without blame, and engage local leaders, schools, markets and refugee/displaced-person services.
Oral cholera vaccine can be used as an additional outbreak/endemic-control tool under national campaign guidance; vaccination does not replace WASH or early treatment.
Use a One Health approach: coordinate clinicians, laboratories, environmental health officers, water authorities, surveillance teams and community leaders.

18. Special populations

Infants and children: weigh if possible, assess tears/feeding/wet nappies, use paediatric weight-based fluids, continue breastfeeding and monitor glucose.
Severe acute malnutrition: signs can be unreliable and standard rapid IV volumes may harm; use the specialised malnutrition protocol and senior review.
Pregnancy: dehydration threatens both mother and fetus; monitor perfusion, fetal status where appropriate and involve obstetric services.
Older adults/heart or renal disease: may decompensate with both dehydration and overhydration; use frequent lung, oxygenation and fluid-balance assessment.
People with disability: adapt communication, provide accessible toilets and do not assume inability to report thirst or pain means low risk.

19. Clinical scenarios

Scenario 1 – alert patient with early cholera. A 24-year-old has six watery stools, thirst and normal blood pressure but is alert and drinking. Move to the designated area, perform triage, start measured ORS, record output, collect a specimen if requested, provide food/water counselling and reassess before discharge.

Scenario 2 – severe dehydration. A 40-year-old arrives lethargic with a weak pulse, cold hands, very little urine and repeated vomiting. Call for resuscitation support, use PPE, check glucose, establish IV/IO access if trained, start protocol-based Ringer's lactate, give ORS as soon as possible, monitor closely and urgently escalate for shock.

Scenario 3 – child with ongoing losses. A 3-year-old improves after oral rehydration but continues passing large stools. Continue breastfeeding and measured ORS, chart every stool/urine, provide paediatric zinc if prescribed, reassess hydration and admit/refer if drinking worsens or perfusion falls.

Scenario 4 – atypical diarrhoea. A patient has watery stool plus high fever, blood, severe focal abdominal pain and guarding. Manage dehydration, isolate appropriately and urgently assess for dysentery, surgical abdomen or another invasive infection rather than assuming uncomplicated cholera.

20. Common errors to avoid

Waiting for a laboratory result before starting ORS or IV fluid.
Giving plain water, soda, juice or overly concentrated homemade salt solution instead of correctly prepared ORS.
Giving antibiotics to every patient while neglecting rehydration and source-control/public-health measures.
Using an unmonitored fluid schedule in a child, malnourished patient, pregnant person or patient with heart/renal disease.
Failing to measure stool, vomit and urine output or to repeat perfusion observations.
Allowing suspected cases to share toilets, buckets, linen, weighing scales or food areas without disinfection.
Using antidiarrhoeal medicines that slow gut motility in a severely ill or febrile patient without senior advice.

CHOLERA emergency check – “DRIP-WASH”
D – Detect dehydration and dangerous alternatives
R – Rehydrate immediately with ORS/IV protocol
I – Isolate and institute PPE/hand hygiene
P – Plot pulse, perfusion, output and response
W – Water, waste and specimen safety
A – Antibiotics only when indicated
S – Support nutrition, breastfeeding and surveillance
H – Health education, household prevention and handover

21. Revision questions

Define cholera and describe its faecal–oral transmission cycle.
Explain how cholera toxin produces profuse watery diarrhoea and hypovolaemic shock.
List the clinical signs of some dehydration and severe dehydration.
What are the priorities during the first five minutes of a patient with cholera shock?
Why is ORS the cornerstone of treatment, and why can plain water be inadequate?
When may antibiotics be considered, and why must they never replace rehydration?
List six infection-prevention measures in a cholera treatment centre.
Give five household actions that interrupt cholera transmission.

22. Key take-home points

Cholera can kill within hours through fluid and electrolyte loss, but correct rehydration is highly effective.
Assess perfusion and mental state repeatedly; blood pressure may remain normal until late shock.
Start ORS immediately when the patient can drink and IV crystalloid immediately for severe dehydration or shock.
Continue breastfeeding and nutrition, measure ongoing losses and monitor urine, glucose and electrolytes.
Antibiotics are selective adjuncts; local protocol and susceptibility data determine the choice.
WASH, hand hygiene, safe stool disposal, surveillance and oral cholera vaccination protect the wider community.

Safety note: This is an educational EMT guide, not a prescription. Fluid volumes, antimicrobial choice, zinc regimen, chlorine concentration and referral thresholds must be checked against the current Uganda Ministry of Health cholera guideline, patient weight, age, pregnancy, malnutrition, organ function and available services.

References for further study

WHO: Cholera fact sheet
CDC: Treating cholera
WHO: Preventing and controlling cholera in endemic countries
WHO: Cholera vaccines and immunization
WHO Africa: Cholera management guidelines
Uganda Ministry of Health: current national cholera case-management, WASH and surveillance guidance.

Cholera in Emergency Care: Rehydration, Shock and Outbreak Management Read More »

Bacterial Infections in Emergency Care: Recognition, Assessment and Management

Why this topic matters. Bacterial disease can progress from a local infection to bacteraemia, sepsis, shock, organ failure and death within hours. Emergency medical technicians (EMTs) are often the first professionals to notice the subtle change: a patient who is newly confused, breathing faster, passing very little urine or becoming cold and mottled. Safe care combines early recognition, infection-prevention precautions, rapid ABCDE assessment, appropriate specimens, timely antimicrobials, source control, careful fluids and continuous reassessment. Always apply the current Uganda Clinical Guidelines, Ministry of Health protocols, antimicrobial formulary and senior-clinician direction.

1. Learning objectives

Define bacterial infection, colonisation, contamination, bacteraemia, sepsis and septic shock.
Recognise common emergency bacterial syndromes and the findings that indicate immediate referral.
Perform a structured history and ABCDE assessment while protecting the patient, team and community.
Obtain useful cultures without delaying life-saving treatment; interpret common laboratory and bedside results.
Describe first aid, pre-hospital care, emergency-department management, nursing care, monitoring and escalation.
Use antibiotics safely: correct indication, agent, route, timing, dose checks, allergy screening, renal review, de-escalation and documentation.
Explain source control, infection prevention, antimicrobial stewardship and prevention of recurrent infection.

2. Core definitions

Term	Meaning and EMT relevance
Colonisation	Micro-organisms are present and multiplying without tissue invasion or symptoms. Colonisation is not automatically an indication for antibiotics.
Contamination	Organisms enter a specimen, wound or surface during collection or handling but are not the cause of disease. Poor sampling can lead to harmful treatment.
Local infection	Invasion of tissue causing pain, heat, swelling, erythema, discharge, cough, dysuria or another site-specific syndrome.
Bacteraemia	Viable bacteria in the bloodstream. It may be transient or may trigger sepsis; blood cultures help identify the organism.
Sepsis	Life-threatening organ dysfunction caused by a dysregulated response to infection. Think infection plus new organ dysfunction, not fever alone.
Septic shock	A severe sepsis state with persistent circulatory/metabolic failure and high mortality; hypotension, poor perfusion, rising lactate and need for vasopressor support are warning signs.
Antimicrobial resistance (AMR)	When organisms no longer respond to medicines that previously worked. Inappropriate antibiotic use, missed doses and poor infection control accelerate AMR.

3. How bacterial infection causes emergency deterioration

Bacteria may remain at the original site, spread through lymphatics or invade the bloodstream. Bacterial toxins and host inflammatory mediators increase vascular permeability, cause vasodilation, disturb coagulation and impair cellular oxygen use. The result can be fever or hypothermia, tachycardia, tachypnoea, capillary-leak oedema, hypotension, delirium, oliguria, hypoxaemia and metabolic acidosis. A patient may be septic even when the temperature is normal.

Local tissue injury: pus, necrosis, abscess formation, cellulitis, consolidation or obstruction.
Systemic inflammation: vasodilation, capillary leak, relative hypovolaemia and increased oxygen demand.
Microcirculatory failure: impaired tissue perfusion despite a seemingly acceptable blood pressure.
Organ dysfunction: altered consciousness, respiratory failure, acute kidney injury, coagulopathy, jaundice or myocardial dysfunction.
Rapid source progression: meningitis, necrotising fasciitis, obstructed pyelonephritis and intra-abdominal sepsis can worsen before obvious external signs develop.

4. Common bacterial emergency syndromes

Syndrome/source	Typical clues	Immediate danger
Sepsis or bacteraemia	Rigors, fever/hypothermia, fast breathing, confusion, mottled skin, weak pulse, oliguria or hypotension.	Septic shock, acute kidney injury, respiratory failure and multiorgan dysfunction.
Meningitis	Fever, severe headache, neck stiffness, photophobia, vomiting, altered consciousness, seizures or non-blanching rash.	Cerebral oedema, seizures, herniation and death; do not delay antibiotics for a difficult lumbar puncture.
Pneumonia	Cough, dyspnoea, pleuritic pain, crackles, hypoxaemia, fever or confusion in an older adult.	Respiratory failure, sepsis, empyema and shock.
Urinary infection/pyelonephritis	Dysuria, frequency, flank pain, fever, rigors, vomiting or catheter-associated symptoms.	Obstructed infected system, urosepsis and renal injury.
Skin, wound or diabetic-foot infection	Redness, warmth, swelling, pain, pus, malodour, ulcer, crepitus or rapidly spreading discoloration.	Necrotising infection, limb loss, tetanus and septic shock.
Intra-abdominal infection	Severe/localised pain, guarding, rebound, distension, vomiting, absent bowel sounds or jaundice.	Perforation, peritonitis, abscess and profound sepsis.
Bone/joint infection	Hot swollen joint, severe movement pain, fever, osteomyelitis risk or prosthesis.	Rapid cartilage destruction, bacteraemia and disability.
Obstetric, neonatal or post-operative infection	Foul lochia, uterine tenderness, wound discharge, poor feeding, hypothermia, lethargy or respiratory distress.	Maternal/neonatal septic shock and rapid deterioration.

5. Triage: identify the patient who cannot wait

Immediate resuscitation and senior review: airway compromise; severe work of breathing or SpO₂ below the local target; systolic hypotension or a weak/absent peripheral pulse; capillary refill markedly prolonged; new confusion, seizure or coma; non-blanching purpura; rapidly spreading soft-tissue pain/swelling; severe dehydration or no urine; lactate elevation; pregnancy with shock; a neonate or immunocompromised patient who looks unwell.

Use an emergency triage category and record the time of arrival, first observations and time of escalation.
Do not be reassured by one normal vital sign. Compare with the patient's baseline and repeat trends.
Check blood glucose early in an altered or shocked patient; treat hypoglycaemia according to protocol while investigating infection.
Separate suspected airborne/droplet disease, cover draining wounds and use standard precautions for every patient.
Arrange a monitored bed and urgent clinician assessment for possible sepsis rather than placing the patient in an unobserved waiting area.

6. Focused history

Presenting illness: onset, progression, fever pattern, rigors, pain site, cough, sputum, dyspnoea, urinary symptoms, diarrhoea, vomiting, rash, wound or discharge.
Severity and function: confusion, fainting, reduced activity, inability to drink, urine volume, breathing effort and ability to walk.
Exposure: sick contacts, crowded housing, healthcare exposure, animals, food/water, travel, flood water, sexual exposure, wounds, injections or recent procedures.
Risk factors: HIV or other immunosuppression, diabetes, malnutrition, pregnancy, extremes of age, sickle cell disease, renal/liver disease, cancer, burns, indwelling devices and recent surgery.
Medicines and microbiology: antibiotics in the last three months, adherence, allergies (reaction and timing), resistant organisms, recent admissions and vaccination status.
Use SAMPLER: Symptoms, Allergies, Medications, Past history, Last oral intake, Events/environment, Risk factors and relevant pregnancy/menstrual history.

7. ABCDE assessment and immediate actions

Step	Look for	Action while escalating
A – Airway	Voice change, secretions, vomiting, facial swelling, reduced consciousness and inability to protect the airway.	Suction, jaw thrust, airway adjunct if trained, lateral position when appropriate, prepare advanced airway support and protect the cervical spine if trauma is possible.
B – Breathing	Rate, effort, chest movement, SpO₂, cyanosis, crackles, wheeze, pleuritic pain and fatigue.	Give oxygen to the prescribed target, position upright, assist ventilation if tiring, monitor continuously and consider pneumonia, sepsis, pulmonary oedema or pneumothorax.
C – Circulation	Pulse, blood pressure, skin temperature/colour, capillary refill, bleeding, dehydration and urine output.	Control bleeding, establish IV/IO access if trained, take cultures without delaying treatment, give cautious isotonic fluid boluses when indicated and reassess lungs, perfusion and response.
D – Disability	AVPU/GCS, pupils, seizures, delirium, meningism and bedside glucose.	Protect from aspiration, treat hypoglycaemia/seizures per protocol, consider meningitis/encephalitis and avoid unsafe lumbar puncture in raised-ICP features.
E – Exposure	Temperature, rash/purpura, wounds, pressure areas, line sites, abdominal tenderness, joints and hidden infection sources.	Expose respectfully, prevent heat loss, mark spreading erythema, photograph only under policy, obtain specimens, then cover and maintain dignity.

8. Investigations and specimen safety

Bedside: repeat vital signs, SpO₂, glucose, urine output, capillary refill and point-of-care lactate where available.
Blood: full blood count, renal/electrolytes, liver tests, glucose, lactate and coagulation when indicated. Take blood cultures from separate sites before antibiotics if this causes no clinically important delay.
Urine: clean-catch or catheter specimen according to protocol; urinalysis and culture when urinary infection is plausible. Do not treat asymptomatic bacteriuria automatically.
Respiratory: chest radiograph or ultrasound when indicated; sputum culture for severe, recurrent or treatment-failure disease; use respiratory isolation when a transmissible syndrome is suspected.
CSF: lumbar puncture only after clinical safety assessment. In suspected bacterial meningitis, draw blood cultures and begin empiric treatment promptly; do not wait for imaging or LP if unsafe or delayed.
Wound/tissue: clean first and obtain deep tissue, aspirate or pus where possible; superficial swabs may reflect colonisation.
Imaging: ultrasound/CT for abscess, obstruction, perforation, deep infection or necrotising process. A normal early image does not overrule a deteriorating patient.

Specimen rule: identify the patient, label at the bedside, record collection time and antibiotics already given, send promptly, and communicate suspected high-risk pathogens to the laboratory before transport.

9. First aid and pre-hospital care

Use gloves and other PPE appropriate to blood, body fluids, respiratory droplets and splash risk; perform hand hygiene before and after contact.
Move the patient from danger, call for backup and start a structured primary survey.
Open and protect the airway, position for breathing, provide oxygen when indicated and assist ventilation if necessary.
Control external bleeding, cover wounds with sterile dressings and do not probe a deep wound in the field.
Keep a septic or shocked patient warm but do not overheat; avoid oral fluids when consciousness or surgery may be a concern.
Check glucose, document vital-sign trends, establish access if trained and arrange early transport to a facility able to provide cultures, antibiotics, surgery and critical care.
Pre-alert the receiving team with suspected source, observations, treatments, allergies, antibiotics already given and estimated arrival time.

10. Emergency treatment principles

10.1 Treat time-critical infection early

When sepsis or a rapidly progressive bacterial syndrome is suspected, obtain cultures promptly if feasible, then give locally recommended empiric antibiotics as soon as possible—especially when shock, meningitis, severe pneumonia, necrotising infection or neutropenia is possible. The prescriber must choose the agent, dose, route and duration using the Uganda Clinical Guidelines, local antibiogram, allergy history, renal/hepatic function, pregnancy status and likely source.

Record exact time of prescription, preparation, administration and any delay.
Check the five rights plus indication, allergy, interactions, dilution, infusion time and compatibility.
Use IV therapy for shock, poor absorption, severe infection or altered consciousness; switch to oral therapy when clinically stable and absorption is reliable.
Review results daily. Narrow, stop or switch treatment when cultures, imaging and clinical progress allow.
Never share leftover antibiotics or encourage patients to stop when they feel slightly better without review.

10.2 Fluids, perfusion and organ support

Assess fluid responsiveness rather than giving unlimited fluid. Use isotonic crystalloid according to local protocol, reassessing blood pressure, pulse, capillary refill, mental state, urine output, lung signs and work of breathing after each bolus.
Use extra caution in heart failure, renal failure, pregnancy, children, severe anaemia and older adults. New crackles, worsening oxygenation or rising work of breathing suggest overload.
If hypotension persists despite appropriate fluid and the facility has capability, urgent senior/critical-care review is needed for vasopressor support and invasive monitoring.
Provide oxygen and ventilatory support, analgesia/antipyretic care, glucose control, renal monitoring and prevention of pressure injury and venous thromboembolism as indicated.

11. Source-specific emergency pathways

11.1 Suspected bacterial meningitis

Isolate appropriately, perform ABCDE and check for rash, seizures, focal deficit, papilloedema, reduced consciousness or shock.
Take blood cultures promptly and begin empiric antibiotics according to age, pregnancy, immune status and local policy. Add other agents only when indicated by local guidance or specialist advice.
Manage seizures, hypoglycaemia, fever and raised intracranial pressure; avoid routine fluid restriction and avoid unsafe LP.
Notify infection-control/public-health teams when a vaccine-preventable or immediately transmissible organism is suspected; assess close contacts for prophylaxis through the appropriate service.

11.2 Pneumonia and lower respiratory infection

Assess respiratory rate, effort, mental state, oxygenation and ability to speak/drink. Silent hypoxaemia or fatigue is an emergency.
Give oxygen to the prescribed target, position upright, suction secretions when required and prepare non-invasive or invasive support if deteriorating.
Look for sepsis, aspiration, tuberculosis, pulmonary oedema and pulmonary embolism; antibiotics should match severity, setting, aspiration risk and local resistance patterns.
Reassess after treatment: rising respiratory rate, increasing oxygen requirement, hypotension, confusion or reduced urine requires escalation.

11.3 Urinary infection and pyelonephritis

Check for flank pain, rigors, vomiting, pregnancy, catheter use, stones and reduced urine.
Take urine culture where indicated and assess for obstruction. An infected obstructed kidney needs urgent urological source control; antibiotics alone may fail.
Give analgesia, antiemetic and carefully monitored fluids; review renal function before nephrotoxic medicines and dose adjustments.

11.4 Skin, wound, diabetic-foot and necrotising infection

Mark the edge of erythema and record pain, colour, temperature, sensation, pulses and function. Pain out of proportion, bullae, crepitus, skin anaesthesia or rapid spread suggests necrotising infection.
Cover wounds, elevate where appropriate, check tetanus status, control glucose and obtain urgent surgical review for abscess, devitalised tissue, deep infection or systemic toxicity.
Do not delay surgery for repeated superficial swabs or a normal early blood test; source control is often the life-saving intervention.

11.5 Intra-abdominal, pelvic and post-operative infection

Keep the patient nil by mouth when surgery is possible, provide IV access, analgesia and antiemetic care, and monitor for peritonitis and shock.
Look for perforation, obstruction, abscess, cholangitis, pelvic infection or an infected wound. Early surgical/obstetric review and source control are essential.
Use pregnancy testing and safeguarding-sensitive history when relevant; avoid exposing a pregnant patient to unnecessary imaging while not delaying life-saving diagnosis.

12. Source control: antibiotics are not enough

Source control means removing, draining, repairing or isolating the cause of infection. Examples include incision and drainage of an abscess, debridement of necrotic tissue, removal/replacement of an infected line, relief of urinary or biliary obstruction, repair of perforation and drainage of an empyema. Escalate early when definitive control is beyond the current facility.

Identify the probable source during the first assessment, then reassess after investigations.
Do not repeatedly delay referral while waiting for antibiotic response in a surgical emergency.
Send deep tissue, pus, blood or fluid for culture at the time of the procedure when safe.
Document the time of source-control consultation and transfer plan.

13. Nursing and EMT care plan

Problem	Interventions	Evaluate
Impaired oxygenation	Position, oxygen/ventilatory support, suction, respiratory observations, aspiration precautions and escalation.	SpO₂ target, respiratory rate/effort, mental state, ABG if available and oxygen requirement trend.
Reduced tissue perfusion	Frequent vitals, IV/IO access, prescribed fluids/vasopressors, warm environment, urine measurement and shock chart.	MAP/BP, pulse quality, capillary refill, skin, mentation, lactate trend and urine output.
Hyperthermia or hypothermia	Temperature schedule, light clothing/blankets, prescribed antipyretic, cultures and review for environmental causes.	Temperature trend, comfort, rigors and response to treatment.
Risk of medication harm	Allergy band, medication reconciliation, independent checks, infusion monitoring and documentation of reactions.	Correct medicine, time, dose, route, renal review and adverse-effect surveillance.
Infection transmission	Hand hygiene, PPE, clean/aseptic technique, equipment decontamination, waste segregation and isolation signage.	Compliance audits, absence of cross-infection and correct specimen transport.
Anxiety, delirium or family distress	Reorient, explain procedures, involve a support person when safe, protect privacy and use interpreters.	Understanding, cooperation, safety and documented communication.

14. Monitoring and escalation

Repeat observations at a frequency matched to severity; unstable patients may need continuous ECG, SpO₂ and frequent blood pressure.
Trend respiratory rate, oxygen requirement, mental status, urine output, capillary refill, lactate and temperature rather than recording isolated values.
Escalate immediately for increasing oxygen need, new confusion, seizure, systolic hypotension, persistent tachycardia, mottling, anuria/oliguria, rising lactate, severe pain out of proportion or a spreading rash.
Use a written handover such as SBAR: Situation, Background, Assessment, Recommendation. Include infection source, cultures, antimicrobial times, fluid balance and response.
After stabilisation, review microbiology, antibiotic spectrum, source control and duration every day; record the review and stop date.

15. Special populations

Children: compensate with tachycardia before hypotension; assess feeding, wet nappies, interaction, capillary refill and weight-based medicines/fluids.
Neonates: temperature instability, poor feeding, lethargy, apnoea or grunting may be the only signs. Urgent neonatal referral is required.
Pregnancy/postpartum: physiological changes can mask shock; consider urinary, uterine, wound and breast sources, and involve obstetric services early.
Older adults: may have no fever; new confusion, falls, weakness or functional decline can be infection signs.
Immunocompromised patients: infection may progress rapidly with minimal local inflammation; do not wait for a high white-cell count.
Renal or hepatic impairment: review dosing, fluid tolerance and nephrotoxic/hepatotoxic combinations with the prescriber or pharmacist.

16. Prevention and antimicrobial stewardship

Vaccination, safe water and food, hand hygiene, respiratory etiquette, wound care, safe sex, vector control and early treatment of chronic disease reduce bacterial emergencies.
Use standard precautions for every patient and transmission-based precautions when indicated; clean shared equipment between patients.
Prescribe antibiotics only for a likely bacterial indication; do not use them for uncomplicated viral respiratory illness.
Follow the WHO AWaRe/local formulary approach: prefer effective Access agents when appropriate, reserve Watch/Reserve agents for clear indications and specialist oversight.
Obtain cultures appropriately, review results, narrow spectrum, convert IV to oral when safe and stop when the planned course is complete.
Teach patients not to share, save or buy antibiotics without assessment, and to return for worsening symptoms or adverse reactions.

17. Clinical scenarios

Scenario 1 – suspected meningococcal disease. A 19-year-old has fever, headache, neck stiffness, confusion and a non-blanching rash. Protect staff, isolate, perform ABCDE, check glucose, obtain blood cultures if this does not delay treatment, alert the senior clinician, start protocol-based empiric therapy promptly and monitor for seizures/shock. Do not wait for a routine LP if it is unsafe.

Scenario 2 – pneumonia with shock. A 68-year-old is confused, RR 34/min, SpO₂ 84% on room air and BP 86/52 mmHg. Sit upright, give oxygen, establish access, check glucose, take cultures where feasible, begin sepsis treatment under protocol, reassess after cautious crystalloid and arrange critical-care referral. Falling oxygenation or worsening fatigue requires ventilatory support.

Scenario 3 – obstructed pyelonephritis. A patient with fever, flank pain, vomiting and a history of stones becomes hypotensive. Treat as possible urosepsis, obtain urine/blood cultures, give prescribed antimicrobials and monitored fluids, check renal function and urgently arrange imaging/urology because drainage may be lifesaving.

Scenario 4 – necrotising soft-tissue infection. Severe pain, fever, rapidly spreading swelling, bullae and skin anaesthesia after a minor wound are present. Do not be reassured by a small skin opening. Cover, provide analgesia, resuscitate, give protocol-based broad empiric therapy after cultures if feasible, and obtain immediate surgical review for debridement.

18. Common errors to avoid

Waiting for fever, hypotension or a positive culture before acting on a deteriorating patient.
Delaying antibiotics for imaging or lumbar puncture when meningitis, shock or necrotising infection is likely.
Giving repeated large fluid boluses without reassessing lungs, perfusion and urine output.
Using a superficial wound swab as proof of the invasive organism.
Continuing broad antibiotics without a culture review, stop date or source-control plan.
Forgetting pregnancy, renal function, allergies, recent antibiotics and local resistance patterns.
Failing to document exact times, trends, handover and response to treatment.

BACTERIAL emergency check – “SOURCE”
S – Spot red flags and sepsis early
O – Oxygen, airway and observations
U – Understand source, exposures and antibiotics
R – Remove/relieve the source; resuscitate and reassess
C – Cultures, correct antimicrobial and communication
E – Escalate, educate and prevent transmission

19. Revision questions

Differentiate colonisation, contamination, local infection, bacteraemia, sepsis and septic shock.
List at least eight red flags that require immediate senior review in a patient with suspected bacterial infection.
Why should cultures be taken before antibiotics when feasible, and why must this never create a dangerous delay?
Describe the ABCDE assessment of a shocked patient with pneumonia.
Explain why an infected obstructed urinary system requires source control.
List the five medication-safety checks that should occur before an IV antibiotic is administered.
What findings suggest necrotising soft-tissue infection rather than uncomplicated cellulitis?
Give five actions that reduce antimicrobial resistance in an emergency unit.

20. Key take-home points

Infection plus new organ dysfunction is an emergency even without high fever.
ABCDE, oxygenation, perfusion, glucose and repeated trends come before a long differential list.
Give appropriate empiric antibiotics promptly when a time-critical bacterial syndrome is suspected, guided by current local policy.
Antibiotics cannot replace drainage, debridement, removal of infected devices or relief of obstruction.
Every dose, specimen, observation, response and escalation should be documented.

Safety note: This is an educational EMT guide, not a substitute for a current Uganda Ministry of Health protocol, facility antimicrobial guideline, prescription or senior clinical decision. Drug choice, dose, duration and referral thresholds must be checked against the patient's age, weight, pregnancy status, allergies, organ function, local resistance data and available services.

References for further study

World Health Organization: Sepsis and antimicrobial resistance resources
WHO AWaRe antibiotic book
CDC Core Elements of Hospital Antibiotic Stewardship
CDC bacterial meningitis information
Uganda Ministry of Health: current Uganda Clinical Guidelines and national antimicrobial-resistance/IPC guidance.

Bacterial Infections in Emergency Care: Recognition, Assessment and Management Read More »

COVID-19: Emergency Assessment, Oxygen Care and Clinical Management

Why emergency teams still need COVID-19 skills. COVID-19 ranges from asymptomatic infection to hypoxaemic pneumonia, thromboembolism, sepsis, myocarditis and multiorgan failure. Risk is shaped by age, pregnancy, vaccination, comorbidities, immune status and time since symptom onset. EMTs must triage safely, measure oxygenation accurately, recognise silent hypoxaemia, prevent transmission and escalate early. Treatment recommendations change with variants, product availability and national policy, so use the current Uganda Ministry of Health and facility protocol.

1. Learning objectives

Describe SARS-CoV-2 transmission, clinical severity categories and risk factors for deterioration.
Perform safe triage, ABCDE assessment, oxygen assessment and infection prevention.
Recognise severe/critical COVID-19, sepsis, ARDS, thromboembolism and cardiac complications.
Explain supportive care, antiviral eligibility, corticosteroid principles and what treatments to avoid.
Plan nursing observations, escalation, rehabilitation, discharge and prevention education.

2. Cause and transmission

COVID-19 is caused by SARS-CoV-2, an enveloped respiratory virus transmitted mainly through infectious respiratory particles and aerosols, especially in crowded or poorly ventilated spaces. Transmission can occur before symptoms and from people with mild or no symptoms. Risk increases with close, prolonged indoor contact, poor ventilation and inadequate masking during high transmission.

Older adults, people with chronic heart/lung/kidney disease, diabetes, obesity, cancer, immune suppression, pregnancy and incomplete vaccination are more likely to develop severe illness, but any person can deteriorate.

3. Clinical severity categories

Category	Typical findings	EMT priority
Asymptomatic/presymptomatic	Positive test without symptoms	IPC, risk assessment, monitoring and public-health advice.
Mild	Fever, sore throat, cough, fatigue, headache, myalgia, anosmia/ageusia, nausea or diarrhoea without hypoxia	Check risk factors, oxygen saturation and ability to drink; safety-net carefully.
Moderate	Clinical or radiographic pneumonia but no severe hypoxaemia	Medical assessment, serial SpO₂/vitals and consideration of eligible antiviral therapy.
Severe	Respiratory rate rise, SpO₂ below target, extensive pneumonia or increased work of breathing	Hospitalise, give oxygen, evaluate sepsis/PE and escalate early.
Critical	ARDS, respiratory failure, shock, cardiac injury, thrombosis, renal failure or multiorgan dysfunction	Resuscitation/ICU, advanced respiratory support and organ-specific care.

4. Initial contact and infection prevention

Screen at entry for respiratory symptoms, exposure, test status and high-risk conditions.
Provide a well-fitting mask to the patient if tolerated; separate from crowded waiting areas.
Perform hand hygiene; use appropriate mask/respirator, eye protection, gown and gloves based on the task and aerosol risk.
Use a well-ventilated area and limit staff in the room; keep a contact/exposure log during high-risk procedures.
Use dedicated or disinfectable equipment and clean high-touch surfaces according to facility policy.

5. Focused history

Day of illness, progression, fever, cough, dyspnoea, chest pain, fatigue, confusion and ability to drink.
Home SpO₂ readings, if available, and whether oxygen was used.
Vaccination, previous COVID-19, recent contact/travel and other respiratory infections.
Age, pregnancy, diabetes, hypertension, heart/lung/kidney disease, obesity, HIV, cancer and immune-suppressive medicines.
Current medicines, anticoagulants, allergies and recent antiviral/corticosteroid use.
Reduced mobility, unilateral leg swelling, pleuritic pain or haemoptysis suggesting pulmonary embolism.

6. ABCDE and oxygen assessment

A – Airway

Assess speech, secretions, fatigue, altered consciousness and aspiration; prepare a controlled airway plan before exhaustion.

B – Breathing

Measure respiratory rate, work of breathing, SpO₂ and mental status. Check probe placement, perfusion, nail products and waveform; repeat abnormal readings.
Give oxygen for hypoxaemia or respiratory distress; escalate from nasal cannula/mask to high-flow or ventilatory support under trained clinicians.

C – Circulation

Assess pulse, BP, capillary refill, hydration, urine output and shock. Avoid unmonitored fluid loading when ARDS or cardiac/renal disease is possible.

D – Disability

Check glucose, AVPU/GCS, delirium and focal signs; consider hypoxia, sepsis, stroke, thrombosis and metabolic causes.

E – Exposure

Inspect for cyanosis, rash, unilateral leg swelling, pressure injury and signs of another infection while maintaining warmth and dignity.

Emergency red flags: SpO₂ below local target, severe breathlessness, RR rapidly rising, cyanosis, inability to speak full sentences, chest pain, confusion, syncope, shock, haemoptysis, unilateral leg swelling, seizures, persistent vomiting or rapid deterioration.

7. Investigations

Test/assessment	What it helps determine	Caution
Serial vitals, SpO₂ and exertional/position response	Trajectory and oxygen requirement	Do not send an unstable patient walking for a test.
Glucose, FBC, electrolytes, renal/liver tests	Comorbidity, organ injury, anaemia, electrolyte effects and medication safety	Repeat based on severity; do not interpret in isolation.
COVID-19 antigen/NAAT testing	Support diagnosis and IPC pathway	A negative test does not exclude early disease when clinical suspicion is high.
Chest X-ray/ultrasound/CT	Pneumonia, oedema, effusion, PE or alternative diagnosis	Stabilise oxygenation first and use IPC during movement.
ECG/troponin, D-dimer/CTPA where indicated	Myocarditis, acute coronary syndrome or pulmonary embolism	Use clinical probability; D-dimer is not a stand-alone diagnosis.
Blood cultures/lactate	Sepsis or bacterial co-infection	Antibiotics are not routine for viral COVID-19 without another indication.

8. Immediate and pre-hospital management

Mask/separate the patient, put on task-appropriate PPE and notify the receiving facility.
Position upright or in a comfortable posture; use awake proning only when alert, supervised and not contraindicated.
Give oxygen for hypoxaemia or respiratory distress and monitor response continuously.
Check glucose and treat hypoglycaemia; assess perfusion and temperature.
Use cautious isotonic fluid for shock/dehydration with lung reassessment; do not delay transfer for nonessential tests.
Do not give antibiotics, corticosteroids or anticoagulants automatically; base them on severity, co-infection and clinician protocol.
Call ahead with SpO₂, oxygen device/flow, vital-sign trends, comorbidities, test status and PPE requirements.

9. Treatment by severity

9.1 Mild disease

Rest, fluids, paracetamol/acetaminophen when appropriate and monitoring for deterioration.
Assess high-risk patients promptly for time-sensitive outpatient antiviral options according to current national availability and eligibility.
Do not use systemic corticosteroids in patients who do not require supplemental oxygen unless another indication exists.
Provide mask/ventilation, hand hygiene, household protection and return precautions.

9.2 Severe or critical disease

Hospitalise, provide oxygen to the recommended target and monitor respiratory effort, SpO₂, blood gases and mental state.
WHO recommends systemic corticosteroids for severe/critical COVID-19 under protocol; do not start them for mild non-hypoxaemic disease.
Consider antiviral therapy and immune-modulating therapy for eligible patients according to current WHO/national guidance, timing, contraindications and availability.
Investigate/treat bacterial sepsis, pulmonary embolism, myocardial injury, acute kidney injury and other complications.
Escalate to high-flow nasal oxygen, non-invasive ventilation or invasive ventilation with trained critical-care staff and aerosol precautions.

10. Respiratory support and proning

Reassess oxygen device fit, flow, respiratory rate, work of breathing and mental status after every change.
Awake proning may improve oxygenation in selected alert patients who can reposition safely; it is not a substitute for escalation.
Use high-flow/non-invasive ventilation only where monitoring, trained staff, oxygen supply and aerosol-risk controls are adequate.
Intubate before catastrophic fatigue when indicated; use a senior airway operator, pre-oxygenation, viral filters and a clear post-intubation plan.
For ARDS, use lung-protective ventilation, appropriate PEEP and prone ventilation under ICU protocol.

11. Complications and advanced care

Complication	Clues	Management direction
ARDS	Increasing oxygen requirement, bilateral infiltrates, severe work of breathing	ICU, lung-protective ventilation, prone positioning and fluid review.
Thromboembolism	Sudden pleuritic pain, unexplained hypoxia, tachycardia, haemoptysis or leg swelling	Urgent diagnostic pathway and anticoagulation only after clinician risk/bleeding assessment.
Sepsis/shock	Hypotension, confusion, cool skin, oliguria, rising lactate	Cultures, antimicrobials for probable co-infection, cautious fluids and vasopressors when indicated.
Cardiac injury	Chest pain, arrhythmia, heart failure or troponin rise	ECG/echo, cardiac and critical-care review.
AKI/metabolic injury	Oliguria, rising creatinine, electrolyte/acid-base changes	Perfusion review, renal-dose medications, avoid nephrotoxins and consider renal support.
Neurological complications	Delirium, stroke, seizures, encephalopathy	Glucose, oxygen, neuro assessment, imaging and specialist management.

12. Medication safety and stewardship

Use only authorised, current antiviral regimens; check symptom onset, renal/hepatic function, pregnancy, interactions and availability.
Systemic corticosteroids are for severe/critical hypoxaemic disease under protocol, not routine mild disease.
Do not use antibiotics solely for a positive COVID-19 test without evidence of bacterial infection.
Assess VTE prophylaxis/anticoagulation according to admission status, bleeding risk, platelet count, renal function and local protocol.
Review chronic medicines, avoid abrupt withdrawal of essential treatment and check for interactions with antivirals.
Paracetamol may relieve fever/pain within safe limits; avoid duplicate combination products and NSAIDs when a bleeding/renal contraindication exists.

13. Nursing care and monitoring

Priority	Care	Escalate when
Oxygenation	Serial SpO₂, respiratory rate/effort, device/flow, ABG when available and response to position	Rising oxygen need, fatigue, cyanosis, confusion or inability to speak
Perfusion	Pulse/BP/capillary refill, temperature, urine output, glucose and fluid balance	Shock, oliguria, rising lactate or worsening mental status
IPC	Hand hygiene, PPE, ventilation, isolation, equipment cleaning and safe waste	PPE breach, exposure or inability to maintain separation
Medication	Timely antiviral/steroid/anticoagulant administration, allergy/interaction checks and adverse-effect monitoring	Hyperglycaemia, bleeding, liver/renal injury, infusion reaction or delirium
Mobility/nutrition	Pressure care, early mobilisation when stable, swallow/nutrition assessment and psychological support	Weakness, falls, delirium, aspiration or persistent functional decline

14. Special populations

Pregnancy: assess maternal oxygenation and fetal wellbeing; involve obstetrics and use pregnancy-appropriate therapies.
Children: most have mild/moderate illness, but monitor for hypoxia, dehydration, pneumonia and MIS-C-like inflammatory illness.
Older adults: delirium, falls, weakness or hypothermia may replace fever and cough.
Immunocompromised: symptoms may be prolonged; specialist antiviral/extended-treatment decisions may be required.
Diabetes/heart/kidney disease: monitor glucose, volume status, renal function and drug interactions carefully.

15. Discharge, isolation and long COVID

Discharge only when oxygenation, work of breathing, hydration, mental state and home support are acceptable.
Give clear instructions on mask use, ventilation, hand hygiene, household protection and current national isolation advice.
Return urgently for worsening breathlessness, chest pain, confusion, blue lips, fainting, low SpO₂, persistent vomiting or reduced urine.
Arrange review for persistent fatigue, breathlessness, chest pain, cognitive symptoms, mood change or reduced exercise tolerance.
Explain vaccination/booster recommendations according to current Uganda policy and individual risk.

16. Clinical scenarios

Scenario 1 – Silent hypoxaemia. A patient with mild cough appears comfortable but SpO₂ is 86% on repeat measurement with good waveform. The EMT confirms probe position, sits the patient upright, applies oxygen, repeats observations, alerts the receiving facility and transfers urgently. Appearance alone is not used to rule out severe disease.

Scenario 2 – Mild COVID-19 with risk factors. A 68-year-old with diabetes presents on day 3 with fever and cough but normal oxygenation. The clinician assesses eligibility and timing for an authorised antiviral, reviews interactions/renal function, provides safety-net advice and arranges follow-up. Steroids are not started simply because the test is positive.

Scenario 3 – Severe disease with shock. A patient with pneumonia becomes confused, hypotensive and oliguric. The team uses PPE, oxygen, ABCDE, glucose, cultures, sepsis management, cautious fluid assessment and early ICU/vasopressor escalation while evaluating bacterial co-infection and thromboembolism.

17. Common errors

Trusting a single normal SpO₂ or visual appearance.
Giving systemic steroids to non-hypoxaemic mild disease.
Prescribing antibiotics automatically for every positive test.
Ignoring PE, myocardial injury, bacterial sepsis or alternative pneumonia.
Overloading a patient with fluids despite ARDS or heart/renal disease.
Performing aerosol-generating procedures without preparation and PPE.
Discharging without oxygen, return precautions, follow-up and household IPC education.

18. Quick revision questions

What distinguishes mild, severe and critical COVID-19?
Why can pulse oximetry be misleading?
List six red flags requiring urgent escalation.
When are systemic corticosteroids indicated?
Why are antibiotics not routine for viral COVID-19?
What complications should EMTs actively screen for?
How should oxygen and respiratory effort be monitored?
Which patients may need time-sensitive antiviral assessment?
What PPE and ventilation measures reduce transmission?
What discharge safety-net advice is essential?

19. Key takeaways

References and further reading

COVID-19: Emergency Assessment, Oxygen Care and Clinical Management Read More »

Rabies: Bite Management, Post-Exposure Prophylaxis and Emergency Care

Why rabies is an emergency. Rabies is a viral encephalitis transmitted mainly through the saliva of infected mammals, especially dogs. Once clinical neurological symptoms appear, rabies is nearly always fatal; before symptoms, prompt post-exposure prophylaxis (PEP) is highly effective. Every EMT must know the first action—immediate, thorough wound washing—and must never reassure a bite victim simply because the wound looks small or the animal ran away.

1. Learning objectives

Explain how rabies is transmitted and why dog vaccination protects people.
Classify animal exposures and identify when vaccine and rabies immunoglobulin (RIG) are indicated.
Perform immediate wound care, bleeding control, tetanus assessment and infection prevention.
Recognise prodromal, furious and paralytic rabies and protect the airway.
Describe PEP, pre-exposure prophylaxis, referral, animal observation and public-health reporting.
Provide detailed nursing, psychosocial, palliative and family care for symptomatic disease.

2. Definition, transmission and burden

Rabies is a zoonotic infection caused by lyssaviruses. Virus in saliva or nervous tissue enters through a bite, scratch, lick on broken skin or exposure of mucous membranes. Dogs cause most human rabies deaths globally, but cats, bats, jackals, foxes, mongooses and other mammals can transmit it. Casual contact, touching fur, feeding an animal or a lick on intact skin is not usually an exposure.

The virus travels along peripheral nerves to the central nervous system. Incubation is commonly weeks to months but can be shorter or longer depending on wound depth, proximity to the brain, viral dose and immune factors. A tiny facial or hand wound can be more dangerous than a larger wound on a distant limb.

Safety rule: treat a credible exposure immediately. Do not wait for symptoms, laboratory confirmation or the animal’s final status before starting the PEP assessment.

3. Exposure categories

Category	Exposure example	Usual PEP implication
Category I	Touching/feeding an animal, lick on intact skin, contact with urine/fur without saliva entering a wound	No PEP if the history is reliable and skin is intact; counsel and document.
Category II	Nibbling uncovered skin, minor scratch or abrasion without bleeding	Immediate wound washing and rabies vaccine assessment under national/WHO protocol.
Category III	Single/multiple transdermal bites or scratches, saliva on broken skin/mucosa, bat exposure or severe facial/hand/genital wounds	Immediate washing, vaccine and RIG when indicated; urgent referral to a PEP centre.

Category assignment can change after careful examination. If the exposure history is uncertain, discuss it with the designated rabies/public-health clinician rather than dismissing risk.

4. First contact: the first 15 minutes

Protect yourself: use gloves for blood and wound fluid; restrain the animal only through trained veterinary/public-health personnel.
Control severe bleeding: apply direct pressure with clean gauze. Do not delay washing once life-threatening bleeding is controlled.
Wash immediately: flush and wash the wound thoroughly with soap or detergent and copious running water for approximately 15 minutes.
Disinfect: if available and compatible with the wound, apply a virucidal iodine-containing or approved antiseptic after washing.
Do not harm the wound: never apply chilli, plant juices, acids, alkalis, ash, soil or other irritants; do not suck the wound.
Do not close immediately: avoid tight primary closure; if closure is essential, use minimal sutures after RIG infiltration and specialist review.
Start the pathway: document the animal, exposure, wound, time and previous rabies vaccination, then arrange same-day PEP assessment.

5. Exposure history and examination

5.1 Animal questions

Species, ownership, vaccination status, location and availability for veterinary observation/testing.
Was the animal behaving abnormally, drooling, restless, paralysed, aggressive or unusually tame?
Was the attack provoked, or was the animal unprovoked and roaming?
Did the animal escape, die, get killed or remain healthy during observation?
Was there contact with a bat, wild carnivore or animal that cannot be observed?

5.2 Patient and wound assessment

Time of exposure, number/depth of bites, scratches, licks, mucosal contact and clothing penetration.
Exact sites: face/scalp/neck, hands/fingers, feet, genitals and other areas.
Bleeding, devitalised tissue, tendon/nerve/vessel/joint injury, foreign body and contamination.
Previous complete rabies vaccination or PrEP, immune suppression, pregnancy, age and tetanus history.
Signs of bacterial infection: increasing redness, warmth, swelling, pus, fever or lymphangitis.

6. Emergency wound and bite management

After washing, assess circulation, sensation, movement and tendon function distal to the wound.
Remove rings, bracelets and tight clothing before swelling increases.
Use sterile non-adherent dressing; elevate when appropriate and provide analgesia.
Assess need for antibiotic prophylaxis/treatment for deep punctures, hand/face wounds, crush injuries, immunocompromise or established infection according to local guidance.
Assess tetanus immunisation and provide vaccine/TIG if indicated by wound type and vaccination history.
Refer hand, face, joint, tendon, nerve, vascular, deep puncture and extensive wounds for surgical review.

7. Post-exposure prophylaxis (PEP)

PEP has three possible components: immediate wound treatment; a WHO-recommended rabies vaccine regimen; and rabies immunoglobulin for category III/qualifying exposures in people not previously adequately vaccinated. Follow the current Ugandan/national protocol and product instructions because intradermal and intramuscular schedules differ.

Wound treatment: wash/flush for about 15 minutes and disinfect.
Vaccine: start as soon as possible at an authorised PEP centre; complete every scheduled dose even if the wound heals or the animal appears well initially.
RIG: for qualifying severe exposures, infiltrate as much as anatomically feasible into and around all wounds; give remaining product only by the approved route and at a separate site from vaccine. Do not inject RIG into the same syringe/site as vaccine.
Previously vaccinated patients: follow the reduced vaccine regimen and do not give RIG unless the national rabies clinician specifically advises otherwise.
Delayed presentation: do not abandon PEP because days have passed; urgently assess and begin the recommended regimen.

8. Vaccine and RIG safety

Record product, batch, dose, route, anatomical site and date for every injection.
Do not give rabies vaccine in the gluteal area; use the approved deltoid/anterolateral-thigh site for the product and patient age.
Observe for immediate allergic reactions and provide clear advice for mild local/systemic reactions.
Do not interrupt the course for minor reactions without clinician review; serious reactions need urgent assessment.
Pregnancy and breastfeeding are not reasons to withhold indicated PEP; seek expert guidance but do not delay.
Immunocompromised patients may need specialist testing or additional doses according to national protocol.

9. Clinical rabies: stages and signs

Stage	Possible findings	Emergency priority
Prodrome	Fever, malaise, headache, anxiety, insomnia, nausea and pain/tingling or itching at the healed bite site	Urgent infectious-disease referral; ask about missed/insufficient PEP.
Furious encephalitic rabies	Agitation, confusion, hallucinations, hyperactivity, hydrophobia, aerophobia, hypersalivation, painful spasms and autonomic surges	Quiet low-stimulation room, airway readiness, sedation and specialist/ICU care.
Paralytic rabies	Ascending flaccid weakness, areflexia, bladder dysfunction and respiratory failure	Support ventilation and distinguish from Guillain–Barré syndrome and spinal disease.
Coma/terminal phase	Progressive encephalopathy, respiratory failure, coma and multiorgan instability	Critical care, family communication and compassionate palliative planning.

Hydrophobia is not ordinary fear of drinking. Painful involuntary throat spasms triggered by attempts to drink or even a breeze may occur with preserved awareness. Avoid forcing oral fluids and protect the patient from aspiration and distress.

10. Management of symptomatic rabies

Admit to a quiet, private, low-stimulation area with infection-control precautions and a senior/ICU team.
Assess airway, breathing, circulation, glucose, seizures, temperature, urine output and autonomic instability repeatedly.
Use oxygen, suction and early airway/ventilation planning; avoid unnecessary procedures that trigger spasms.
Provide carefully titrated sedation/analgesia and treatment of spasms under critical-care/infectious-disease guidance.
Do not force oral food, water or medication when hydrophobia, dysphagia or altered consciousness is present; use a safe nutrition/medication route.
Manage secretions, aspiration, urinary retention, pressure injury, thrombosis, electrolyte imbalance and pain.
Discuss prognosis, goals of care and palliative support sensitively with the family; once clinical symptoms develop, survival is extraordinarily rare.

11. Infection prevention and staff safety

Use standard precautions for saliva, blood, urine and respiratory secretions; gloves and eye protection are needed for splash risk.
Human-to-human transmission is exceptionally rare outside organ/tissue transplantation, but avoid saliva contact and use safe suction/sharps practice.
Clean and disinfect equipment, contain secretions and dispose of sharps safely.
Staff bitten or exposed to saliva on broken skin/mucosa need immediate washing and urgent occupational-health PEP assessment.
Do not kill, handle or transport a suspect animal without veterinary/public-health coordination.

12. Nursing care plan

Problem	Interventions	Escalate when
Airway/aspiration risk	Quiet environment, suction ready, side positioning when safe, NPO if unsafe swallow and respiratory observations	Stridor, laryngospasm, pooling saliva, cyanosis or falling consciousness
Hydrophobia/agitation	Dim room, limit visitors/noise, explain before touching, prescribed sedation and family support	Uncontrolled spasms, autonomic crisis, injury or severe distress
Wound care	Document site/measurements, aseptic dressing, neurovascular checks, analgesia and antibiotic/tetanus plan	Progressive infection, tissue loss, neurovascular deficit or compartment concern
Nutrition/fluid balance	Swallow review, safe enteral/parenteral plan, urine/stool chart and oral care	Dehydration, aspiration, retention, oliguria or electrolyte disturbance
Psychosocial care	Support child/family, explain PEP schedule, protect confidentiality and provide grief/palliative support when needed	Missed PEP doses, caregiver distress or safeguarding concerns

13. Animal observation and public-health coordination

Record species, owner, vaccination record, location, behaviour and circumstances of attack.
Notify the designated veterinary/public-health team so the animal can be observed, tested or safely managed.
Never delay indicated PEP while waiting for an animal observation decision.
Trace other people exposed to the same animal and link them to PEP services.
Report clusters, unusual animal deaths and unvaccinated roaming dogs through the One Health pathway.

14. Prevention and One Health

Vaccinate dogs and cats, control roaming animals humanely and improve access to veterinary services.
Teach children not to approach, tease, feed or handle unfamiliar animals.
Keep pets supervised, vaccinated and safely confined; report abnormal animal behaviour.
Make wound-washing materials, vaccines and RIG accessible in rural and urban facilities.
Provide pre-exposure vaccination for selected high-risk workers such as veterinarians, animal handlers, laboratory staff and some travellers.
Use community education so families do not apply irritants or wait for symptoms after a bite.

15. Clinical scenarios

Scenario 1 – Child bitten by a roaming dog. A 9-year-old has a bleeding calf wound from an unknown dog that escaped. The EMT controls bleeding, washes/flushes for 15 minutes, disinfects, assesses the wound and tetanus status, documents the animal and urgently refers for category III PEP assessment. The team does not wait to see whether the dog returns.

Scenario 2 – Saliva on broken skin. A farmer has a scratch from a sick cat with saliva contamination. The EMT washes immediately, avoids irritants and tight closure, arranges vaccine/RIG assessment under the national category pathway, and notifies veterinary/public health.

Scenario 3 – Hydrophobia and spasms. A patient presents with fever, tingling at an old bite site, fear of water, throat spasms and agitation. The EMT reduces stimulation, protects the airway, avoids forced oral fluids, calls the infectious-disease/ICU team and provides compassionate family communication. PEP is preventive and cannot be relied on after clinical disease begins.

16. Common errors

Closing or suturing a bite before thorough washing and RIG assessment.
Applying chilli, herbs, ash, acids or other irritants to the wound.
Waiting for the animal, laboratory test or symptoms before starting PEP assessment.
Giving RIG in the same site/syringe as vaccine or failing to infiltrate wounds.
Stopping vaccine because the wound looks healed or a mild reaction occurs.
Forcing water into a hydrophobic patient or creating unnecessary stimulation.
Ignoring tetanus, bacterial infection, tendon injury or rabies exposure among staff.

17. Quick revision questions

What is the first action after a suspected rabies exposure?
Differentiate category I, II and III exposures.
When is RIG indicated and where should it be placed?
Why must PEP begin before symptoms?
What questions help assess the animal?
List six signs of clinical rabies.
How should a hydrophobic patient be positioned and supported?
Which other wound-care measures are needed besides PEP?
What should happen to staff exposed to saliva?
List five One Health prevention strategies.

18. Key takeaways

References and further reading

Rabies: Bite Management, Post-Exposure Prophylaxis and Emergency Care Read More »

Tetanus: Emergency Recognition, Spasm Control and Prevention

Why tetanus is preventable but dangerous. Tetanus toxin causes painful muscle rigidity, stimulus-triggered spasms, laryngospasm, autonomic instability and respiratory failure. It is a clinical diagnosis and a medical emergency; a negative culture does not rule it out. Treatment combines hospital/ICU care, wound debridement, tetanus immune globulin (TIG), antibiotics, spasm control, airway support and active vaccination. Prevention depends on clean wounds, clean birth/cord care and complete tetanus-toxoid-containing vaccination.

1. Learning objectives

Explain the cause, incubation and forms of tetanus.
Recognise trismus, risus sardonicus, generalized spasms and autonomic dysfunction.
Assess airway, breathing, circulation, wounds and triggers without provoking spasms.
Describe wound management, TIG, antibiotics, sedation, ventilation and nutrition.
Plan nursing care, environmental control, rehabilitation and prevention.
Apply wound prophylaxis principles for patients with unknown or incomplete vaccination.

2. Cause and pathophysiology

Tetanus is caused by neurotoxin produced by Clostridium tetani spores that enter a wound. Spores survive in soil, dust and animal/human faeces and germinate in low-oxygen tissue such as punctures, crush injuries, burns, necrotic wounds, injection sites, chronic ulcers or an infected umbilical stump. Tetanospasmin travels to the nervous system and blocks inhibitory neurotransmitters, producing unopposed muscle contraction and autonomic overactivity.

Tetanus is not normally transmitted person-to-person, and illness does not produce reliable natural immunity. A recovered patient still needs vaccination.

3. Forms and incubation

Form	Clinical pattern	Emergency concern
Generalized tetanus	Trismus, risus sardonicus, neck/back rigidity, painful generalized spasms and opisthotonus	Laryngospasm, respiratory failure, aspiration, fractures and autonomic crisis.
Local tetanus	Persistent rigidity/spasm near the wound	May progress to generalized disease; requires observation and treatment.
Cephalic tetanus	Cranial nerve palsies after head/face injury or otitis	Rapid progression and airway/bulbar risk.
Neonatal tetanus	Normal feeding initially, then poor suck, irritability, rigidity and stimulus-triggered spasms within the first weeks	Severe respiratory failure; urgent neonatal intensive care and maternal/newborn public-health response.
Incubation	Often around 3–21 days, but variable; shorter incubation or close wound-to-brain distance suggests severe disease	Ask the date and type of every possible wound or delivery/cord event.

4. Clinical features and severity

Early: stiffness of jaw/neck, difficulty swallowing, abdominal rigidity, anxiety and muscle pain.
Characteristic: trismus/lockjaw, risus sardonicus, rigid abdomen and painful generalized spasms triggered by light, sound, touch or procedures.
Respiratory: dysphagia, aspiration, laryngospasm, chest-wall rigidity, apnea and fatigue.
Autonomic: labile hypertension/hypotension, tachycardia/bradycardia, sweating, fever, ileus and urinary retention.
Complications: pneumonia, rhabdomyolysis, fractures, pressure injury, venous thromboembolism and malnutrition.

Emergency trigger: any patient with trismus plus painful spasms, dysphagia or a recent contaminated wound needs urgent hospital assessment—even if the temperature and oxygen saturation are normal.

5. Initial contact and ABCDE

A – Airway

Keep the room quiet and dim; avoid unnecessary touch. Assess secretions, swallowing, voice and laryngospasm. Prepare suction and an experienced airway team before spasms become uncontrollable.

B – Breathing

Monitor respiratory rate, effort, SpO₂, cough and chest movement. Spasms can cause sudden hypoxia; oxygen and assisted ventilation may be required.

C – Circulation

Check pulse/BP continuously in severe disease, assess autonomic instability and dehydration, and obtain access gently.
Avoid provoking spasms during procedures; use analgesia/sedation per protocol.

D – Disability

Assess consciousness, spasms, pain, glucose, pupils and injury. Consciousness is often preserved, which can cause severe fear.

E – Exposure

Search for puncture, crush, burn, injection, surgical, dental, obstetric and umbilical wounds. Do not aggressively probe a wound before adequate analgesia/sedation and surgical review.

6. Differential diagnosis

Condition	Overlap	Clue against/for tetanus
Strychnine poisoning	Severe stimulus-triggered spasms	Very rapid onset, preserved relaxation between spasms and exposure history; requires toxicology input.
Meningitis/encephalitis	Fever, rigidity, altered status	Headache/meningism and altered consciousness predominate rather than clear trismus with stimulus spasms.
Hypocalcaemic tetany	Spasm and muscle cramps	Carpopedal spasm, paresthesia and abnormal calcium; check electrolytes.
Rabies	Dysphagia and spasms	Animal exposure, hydrophobia/aerophobia, encephalitis and behavioural change.
Drug-induced dystonia/NMS	Rigidity and autonomic signs	Recent dopamine-blocking drug, hyperthermia and altered mental status.

7. Immediate hospital treatment

Admit to a quiet, low-stimulation monitored area; severe disease needs ICU capability.
Give human tetanus immune globulin promptly under local protocol to neutralise unbound toxin; it cannot reverse toxin already bound to nerves.
Debride and clean the wound thoroughly once airway/spasm control and analgesia are established; remove foreign/necrotic material.
Give antibiotics active against C. tetani according to Uganda/facility guideline and allergy/renal status; antibiotics do not replace TIG or wound care.
Control spasms with benzodiazepines and other ICU medicines under continuous respiratory monitoring; avoid abrupt stimulation.
Vaccinate with a tetanus-toxoid-containing vaccine when clinically stable; disease itself does not confer immunity.

8. Spasm, airway and autonomic management

Reduce noise, bright light, unnecessary handling, suctioning and repeated procedures.
Use prescribed sedation/analgesia and titrate to stop dangerous spasms while preserving safe ventilation when possible.
Prepare early for intubation/tracheostomy and mechanical ventilation if laryngospasm, aspiration, recurrent apnea, exhaustion or uncontrolled spasms develop.
Manage dysautonomia in ICU with continuous ECG/BP, fluid assessment and specialist vasoactive therapy.
Prevent aspiration, pressure injury, DVT, contractures, constipation, urinary retention and ventilator-associated pneumonia.

9. Wound prophylaxis after injury

Wound/record	Core action	Reminder
Clean, minor wound; documented complete primary series	Assess time since last booster and give vaccine if due under current schedule	Clean wound care still matters.
Dirty/deep/puncture/crush/burn/fecal-saliva contaminated wound	Urgent cleaning/debridement; vaccine and TIG may both be indicated when the series is incomplete/unknown	Use the current national table; do not guess from memory.
Unknown history	Treat as not reliably immunised until records are verified; provide indicated vaccine/TIG	Document product, dose, route and follow-up schedule.
Established clinical tetanus	Hospital care, therapeutic TIG, wound care, antibiotics, spasm control and vaccination during recovery	Prophylaxis rules differ from treatment of disease.

10. Neonatal and maternal tetanus

Neonatal tetanus often follows unclean delivery or cord care in a baby whose mother lacked adequate tetanus vaccination.
Signs include inability to suck, irritability, facial grimace, stiffness and spasms triggered by handling or feeding.
Provide quiet NICU-level care, airway/ventilation support, TIG, antibiotics, nutrition and spasm control under paediatric protocol.
Notify maternal/newborn surveillance and assess the mother’s immunisation, delivery and cord-care history.
Prevent cases through antenatal vaccination, skilled clean delivery, sterile cord care and community education.

11. Nursing interventions

Priority	Care	Escalate when
Airway/respiratory	Quiet room, suction, oxygen, respiratory observations and ventilator care if needed	Laryngospasm, cyanosis, weak cough, apnea or rising CO₂
Spasm control	Cluster care, dim lights, gentle touch, prescribed sedation and seizure/spasm chart	Increasing frequency/severity or injuries despite treatment
Autonomic function	Continuous ECG/BP in severe disease, temperature, fluid balance and bowel/bladder chart	Labile BP, dysrhythmia, fever, ileus or urinary retention
Nutrition/swallow	Swallow assessment, aspiration precautions, enteral/parenteral nutrition plan	Choking, recurrent aspiration, severe weight loss or ileus
Wound/skin	Aseptic dressing, debridement support, pressure care, passive movement and DVT prevention	Necrosis, spreading infection, pressure injury or limb compromise

12. Prevention and education

Complete routine childhood tetanus-containing vaccination and boosters according to national schedule.
Vaccinate women of reproductive age/pregnant women and strengthen antenatal follow-up.
Clean wounds promptly with safe water/soap, remove foreign material and seek assessment for deep/dirty injuries.
Use sterile instruments for injections, surgery, dental care and umbilical cord cutting/dressing.
Do not apply soil, ash, dung, herbs or unsterile substances to wounds or umbilical stumps.
Explain that tetanus recovery does not produce immunity; future vaccination remains necessary.

13. Clinical scenarios

Scenario 1 – Puncture wound and unknown vaccine history. A farm worker has a deep nail puncture, trismus and painful spasms. The EMT reduces stimulation, protects the airway, checks observations and arranges urgent hospital care. The team does not simply give an antibiotic and discharge; established tetanus requires TIG, wound debridement, spasm control, vaccination and monitoring.

Scenario 2 – Neonatal tetanus. A 10-day-old who was feeding normally becomes unable to suck and spasms when handled. The EMT minimises stimulation, supports oxygen/ventilation, keeps the baby warm, calls neonatal care and public health, and asks about maternal vaccine and cord-care practices.

Scenario 3 – Dirty wound prophylaxis. A patient presents after a contaminated crush injury with no vaccine record but no tetanus symptoms. The team performs wound care and follows the current vaccine/TIG prophylaxis table. Prevention is still possible because clinical disease has not developed.

14. Common errors

Provoking spasms with bright lights, loud voices or repeated unnecessary procedures.
Waiting for culture results or a visible wound before treating clinical tetanus.
Giving antibiotics without TIG, wound debridement or vaccination.
Underestimating laryngospasm and respiratory failure when SpO₂ is initially normal.
Forgetting to prevent aspiration, pressure injury, DVT and malnutrition during prolonged ICU care.
Assuming a survivor is immune and omitting vaccination.

15. Quick revision questions

How does tetanospasmin produce rigidity and spasms?
List the characteristic clinical signs of generalized tetanus.
What triggers should be minimised?
Why are TIG and vaccination both needed?
What wound types are tetanus-prone?
Which findings suggest impending respiratory failure?
How is neonatal tetanus prevented?
What should the nurse monitor for autonomic instability?
Why does tetanus not confer natural immunity?
Give five discharge/prevention messages.

16. Key takeaways

References and further reading

Tetanus: Emergency Recognition, Spasm Control and Prevention Read More »

Botulism: Recognition, Airway Management and Emergency Care

Why botulism must be recognised early. Botulism is a neuroparalytic emergency caused by botulinum neurotoxin. It produces cranial-nerve palsies followed by symmetrical descending flaccid paralysis and respiratory failure. Fever and sensation are often normal, so the patient may look deceptively stable until ventilation fails. Antitoxin neutralises toxin that has not yet bound to nerve endings; it cannot reverse established paralysis. Give supportive airway/ventilator care and activate the public-health/antitoxin pathway immediately when the clinical picture fits.

1. Learning objectives

Describe foodborne, wound, infant, iatrogenic and inhalational botulism.
Recognise the descending pattern, autonomic signs and respiratory warning features.
Differentiate botulism from stroke, myasthenia gravis, Guillain–Barré syndrome, organophosphate poisoning and diphtheria.
Perform serial airway, breathing, bulbar and neurological assessments.
Explain antitoxin activation, ventilation, nutrition, wound care and rehabilitation.
Implement outbreak notification, contact advice and food-safety prevention.

2. Definition and toxin action

Botulism is illness caused by botulinum neurotoxin produced by Clostridium botulinum and related organisms. The toxin blocks acetylcholine release at neuromuscular junctions and autonomic nerve terminals, causing cranial neuropathies, symmetrical weakness and paralysis. Sensation and consciousness are usually preserved unless hypoxia, sedation or another process occurs.

Types include foodborne botulism from preformed toxin, wound botulism from contaminated tissue, infant botulism from intestinal colonisation, iatrogenic botulism after excessive therapeutic/cosmetic toxin and rare inhalational or deliberate exposure.

3. Typical clinical pattern

Stage/sign	Findings	Emergency meaning
Gastrointestinal prodrome	Nausea, vomiting, abdominal pain, diarrhoea or constipation	May precede neurological signs in foodborne disease; dehydration can coexist.
Cranial nerve involvement	Blurred/double vision, ptosis, dilated or fixed pupils, dry mouth, dysarthria, dysphagia and facial weakness	Bulbar weakness predicts aspiration and respiratory failure.
Descending paralysis	Neck and upper-limb weakness followed by trunk and lower-limb weakness; symmetrical and flaccid	Trend forced vital capacity/respiratory effort and prepare early airway support.
Autonomic dysfunction	Dry mouth, ileus, constipation, urinary retention, orthostatic hypotension, fixed pupils or fluctuating BP	Monitor aspiration, ileus, dysrhythmia and haemodynamic instability.
Respiratory failure	Weak cough, shallow breathing, fatigue, hypercapnia, inability to count/speak or swallow secretions	Intubation and mechanical ventilation may be needed for weeks.

Pattern recognition: acute bilateral cranial neuropathies plus symmetrical descending weakness with clear sensation should trigger immediate botulism consultation—even before laboratory confirmation.

4. History and exposure assessment

Exact onset and sequence of gastrointestinal, visual, bulbar and limb symptoms.
Shared meals, home-canned/preserved/fermented food, smoked fish, honey or food from an outbreak.
Contaminated wound, injection drug use, skin popping, recent surgery or traumatic puncture.
Recent cosmetic or therapeutic botulinum-toxin injections and dose/site.
Infant age, constipation, poor feeding, weak cry, hypotonia and exposure to honey/soil dust.
Medication and toxin history: magnesium, aminoglycosides, sedatives, organophosphates and other neuromuscular blockers.
Contacts who ate the same food or share an injection source.

5. Initial contact and ABCDE

A – Airway and bulbar function

Ask the patient to speak, swallow and cough. Look for pooling saliva, nasal speech, weak gag, dysphagia and aspiration.
Keep suction ready, position safely and involve an experienced airway team early; do not wait for complete paralysis.

B – Breathing

Measure respiratory rate, depth, SpO₂, ability to count aloud, cough strength, chest movement and fatigue. Pulse oximetry can remain normal until late; assess ventilation and blood gas when available.

C – Circulation

Check pulse, blood pressure, postural symptoms, dehydration, ileus and autonomic instability. Use cautious fluids and monitor aspiration/urine output.

D – Disability

Document pupils, ptosis, extraocular movements, facial movement, speech, neck flexion, limb power and reflexes. Check glucose and consider alternative diagnoses.

E – Exposure

Inspect wounds, injection sites, pressure areas and evidence of food poisoning; use standard precautions and preserve food/vomitus samples for public-health teams only when instructed.

6. Respiratory failure: when to intubate or ventilate

Do not rely on SpO₂ alone. A botulism patient can have severe hypoventilation with a deceptively normal oxygen saturation, especially when receiving supplemental oxygen.

Progressive dysphagia, weak cough, inability to handle secretions, recurrent aspiration or rapidly worsening bulbar weakness.
Shallow breathing, rising PaCO₂, respiratory acidosis, declining vital capacity or inability to count/speak in full phrases.
Fatigue, paradoxical breathing, cyanosis, altered consciousness or haemodynamic instability.
Prepare controlled intubation with the most experienced operator, suction and a difficult-airway plan; avoid unnecessary sedatives and neuromuscular blockers unless the airway team directs them.
Mechanical ventilation may be prolonged; plan humidification, pressure injury prevention, secretion care, nutrition and weaning assessment.

7. Differential diagnosis

Condition	Similarities	Distinguishing clues
Myasthenia gravis crisis	Bulbar/respiratory weakness	Fluctuation/fatigability, ocular signs, autoimmune history; botulism has autonomic/GI exposure pattern.
Guillain–Barré syndrome	Progressive weakness and respiratory failure	Usually ascending weakness with sensory symptoms/areflexia; cranial signs can occur but exposure pattern differs.
Brainstem stroke	Diplopia, dysarthria, dysphagia	Sudden focal/asymmetric findings and vascular risk; urgent imaging pathway.
Organophosphate poisoning	Weakness and respiratory failure	Cholinergic excess: salivation, sweating, miosis, diarrhoea and fasciculations—not dry autonomic state.
Diphtheria/tetanus or toxic neuropathy	Bulbar signs, weakness or spasms	Vaccination, wound, rigidity/spasm, sore throat or toxin exposure history.

8. Immediate hospital management

Admit to a monitored area with airway/ventilator capability; notify infectious disease, critical care and public health.
Request botulinum antitoxin immediately through the authorised national/public-health pathway based on clinical suspicion; do not wait for laboratory confirmation.
Collect serum/stool/food or wound specimens only with specialist and laboratory instructions; antitoxin should not be delayed for sampling.
Provide early airway protection, mechanical ventilation and aspiration precautions when bulbar/respiratory function declines.
Perform wound exploration/debridement and appropriate antimicrobial therapy for wound botulism under surgical/infectious-disease guidance.
Give careful fluids, manage ileus/urinary retention, correct electrolytes and provide nutrition via a safe route.

9. Botulinum antitoxin

Antitoxin neutralises circulating toxin and prevents progression; it does not reverse paralysis already established.
Early administration is most effective, but patients may benefit later while new toxin remains in circulation.
Administration must be supervised by a trained clinician because equine-derived products can cause hypersensitivity/anaphylaxis and delayed serum sickness.
Observe airway, blood pressure, rash, wheeze and infusion reaction; have emergency anaphylaxis medicines/equipment ready.
Infant botulism uses a specific human antitoxin pathway where available; contact the designated public-health/paediatric service urgently.

10. Nutrition, gut and urinary care

Keep nil by mouth when swallowing is unsafe; assess gag and speech before oral intake.
Use enteral feeding when the airway is protected and gut motility permits; consider post-pyloric/alternative nutrition with ICU input.
Monitor abdominal distension, bowel sounds, constipation, ileus, vomiting and aspiration risk.
Assess urinary retention and catheterise only when indicated with aseptic technique.
Provide oral care, eye lubrication for incomplete eyelid closure and pressure-area care during prolonged paralysis.

11. Nursing management and rehabilitation

Priority	Interventions	Escalate when
Airway/ventilation	Serial respiratory effort, cough, secretion load, ABG/vital capacity where available, suction and ventilator care	Weak cough, rising CO₂, fatigue, aspiration or increasing support
Bulbar dysfunction	Swallow assessment, NPO if unsafe, aspiration precautions, speech/feeding review	Choking, wet voice, recurrent aspiration or inability to clear secretions
Autonomic instability	Continuous BP/ECG as needed, bowel/bladder chart, hydration and temperature monitoring	Arrhythmia, severe hypertension/hypotension, ileus or retention
Immobility	Two-hourly pressure care, passive range of motion, DVT/contracture prevention and physiotherapy	Skin breakdown, limb swelling, pain or loss of function
Communication/psychology	Explain that consciousness may be preserved, provide communication board and family support	Anxiety, delirium, depression or inability to communicate needs

12. Public-health response and contacts

Notify the designated public-health authority immediately; botulism may signal a foodborne outbreak or deliberate contamination.
List everyone who ate the suspected food, shared a meal or had a common injection source; do not discard food until instructed.
Contacts should receive risk assessment and symptoms education; asymptomatic exposed people need public-health advice rather than unsupervised antitoxin.
Botulism is not usually spread person-to-person, but body-fluid, wound and food-handling precautions still apply.

13. Prevention

Use safe pressure-canning, adequate cooking and refrigeration; discard bulging, leaking or foul-smelling containers.
Do not feed honey to infants under 12 months; prevent soil/dust ingestion.
Clean and debride contaminated wounds promptly; avoid injection drug use and use sterile equipment in healthcare.
Use botulinum toxin only from authorised products and trained practitioners; respect dose and interval limits.
Teach families to seek emergency care for double vision, drooping eyelids, swallowing difficulty, weak voice or breathing problems after a shared meal or injection.

14. Clinical scenarios

Scenario 1 – Foodborne cluster. Several adults develop vomiting, blurred vision, dry mouth and difficulty swallowing 24 hours after a shared preserved meal. The EMT recognises a possible outbreak, checks airway and respiratory effort, keeps patients under observation, calls public health/antitoxin services and transfers the weakest patient with airway support ready. No one waits for laboratory confirmation before requesting antitoxin.

Scenario 2 – Wound botulism. A person who injects drugs has a painful necrotic wound, ptosis, dysarthria and weak cough. The priorities are airway preparation, serial ventilation assessment, urgent antitoxin consultation, surgical source control and protocol-directed antibiotics.

Scenario 3 – Infant botulism. A 4-month-old has constipation, poor feeding, weak cry, hypotonia and shallow breathing. The EMT supports airway/ventilation, prevents aspiration, calls paediatrics/public health for human antitoxin and avoids oral feeding until a swallow plan is established.

15. Common errors

Waiting for paralysis or a positive toxin test before requesting antitoxin.
Assuming a normal SpO₂ excludes respiratory failure.
Giving oral food/medicines to a patient with bulbar weakness.
Missing autonomic signs, constipation or urinary retention.
Using sedatives or neuromuscular blockers without an airway plan.
Failing to notify public health about a foodborne cluster.
Discarding suspected food before it can be investigated safely.

16. Quick revision questions

What is the typical direction of botulism paralysis?
Name five cranial-nerve signs.
Why is antitoxin given before laboratory confirmation?
Which respiratory findings require early intubation planning?
How does botulism differ from organophosphate poisoning?
What are the main botulism exposure routes?
What nursing measures prevent aspiration and pressure injury?
What should happen to people who ate the same food?
Why is infant honey avoidance important?
List four common emergency errors.

17. Key takeaways

References and further reading

Botulism: Recognition, Airway Management and Emergency Care Read More »

Septic Shock: Recognition, Resuscitation and Definitive Management

Why septic shock is time-critical. Septic shock is infection-associated circulatory and cellular/metabolic failure. It can begin with fever, fast breathing, confusion or a subtle change in behaviour and progress to refractory hypotension, kidney injury, respiratory failure and death. Early recognition, appropriate antimicrobials, source control, cautious fluid resuscitation, vasopressor support and frequent reassessment are the core emergency actions. Use the current Uganda Clinical Guidelines, facility sepsis pathway and the latest Surviving Sepsis Campaign guidance.

1. Learning objectives

Define infection, sepsis, septic shock and multiple-organ dysfunction.
Recognise occult hypoperfusion, shock and rapidly deteriorating infection.
Apply an initial ABCDE and sepsis bundle without delaying life-saving treatment.
Describe cultures, empiric antimicrobials, fluids, vasopressors and source control.
Monitor response using perfusion, lactate, urine output, mental status and respiratory findings.
Plan nursing care, antimicrobial stewardship, prevention, referral and post-sepsis recovery.

2. Definitions

Sepsis is life-threatening organ dysfunction caused by a dysregulated response to infection. Septic shock is a severe sepsis state with persistent circulatory/metabolic abnormalities and inadequate tissue perfusion despite appropriate initial resuscitation, requiring vasopressors and intensive monitoring. A patient may have sepsis without fever, positive cultures or obvious hypotension.

Common sources include pneumonia, urinary infection, abdominal infection, meningitis, skin/soft-tissue infection, obstetric infection, infected devices and bloodstream infection. Malaria, dengue, VHF and fungal disease can produce sepsis-like shock and must be considered in Uganda.

Do not use a normal blood pressure to rule out sepsis. Tachypnoea, altered mentation, prolonged capillary refill, cool skin, oliguria or rising lactate can reveal hypoperfusion before hypotension.

3. Pathophysiology and stages

Stage	Physiology/clinical pattern	Priority
Infection with systemic response	Fever or hypothermia, tachycardia, tachypnoea, pain, malaise and inflammatory signs	Find source, measure vitals and identify risk factors.
Early compensated sepsis	Warm peripheries or bounding pulse, fast breathing, confusion, reduced urine or rising lactate	Begin sepsis assessment and treatment before decompensation.
Decompensated shock	Hypotension, cold mottled skin, weak pulse, delayed capillary refill, oliguria and altered consciousness	Resuscitation, antimicrobials, fluids, source control and urgent escalation.
Refractory/multiorgan failure	Persistent vasopressor need, severe acidosis, respiratory/renal/hepatic failure, coagulopathy or coma	ICU/critical care, organ support, prognosis and family communication.

4. Initial recognition and screening

Suspect infection from history, focal symptoms, devices, wounds, pregnancy/postpartum status or epidemiology.
Look for organ dysfunction: confusion, hypotension, hypoxia, oliguria, jaundice, thrombocytopenia, severe pain, acidosis or rising creatinine.
Use an early-warning score or local sepsis screen as an aid—not as a substitute for clinical judgement.
Check serial respiratory rate, pulse, blood pressure, capillary refill, temperature, SpO₂, glucose, mental status and urine output.

High-risk warning signs: respiratory rate ≥22/min or rapidly rising, altered mental state, systolic hypotension, narrow pulse pressure, cool mottled skin, capillary refill >3 seconds, urine <0.5 mL/kg/hr, lactate elevation, hypoxia, cyanosis, severe rigors, purpura, severe pain or rapid deterioration.

5. Immediate ABCDE actions

A – Airway

Assess speech, secretions, vomiting, consciousness and aspiration risk. Prepare suction and an experienced airway plan for exhaustion or reduced consciousness.

B – Breathing

Give oxygen for hypoxaemia or respiratory distress, assess pneumonia/ARDS and prepare assisted ventilation if fatigue develops.

C – Circulation

Obtain reliable IV access, blood samples and cultures when safe; use an intraosseous route if access is urgently impossible.
Assess perfusion before and after every fluid bolus: capillary refill, pulse, mental status, skin, lung sounds and urine output.

D – Disability

Check glucose, AVPU/GCS and pupils; treat hypoglycaemia and seizures immediately.

E – Exposure

Search for pneumonia, urine infection, wounds, devices, meningitis, abdominal/perineal infection, obstetric source and tropical infections; maintain warmth and dignity.

6. First-hour sepsis bundle

Recognise and call: alert the senior clinician, sepsis team and receiving ICU/transfer service.
Measure lactate where available and repeat if elevated or the patient deteriorates.
Take cultures: blood cultures and source-specific specimens before antibiotics when this does not create a dangerous delay.
Give appropriate antimicrobials: start promptly for septic shock/high-probability sepsis using local formulary and resistance data.
Give crystalloid for hypoperfusion: use a measured bolus and reassess for response and overload; individualise in heart/renal failure, pregnancy, dengue or haemorrhage.
Start vasopressor support: if hypotension persists, use norepinephrine first-line in adults under critical-care protocol; do not wait for a central line if delay is dangerous and trained peripheral administration is available.
Find and control the source: drain pus, remove infected devices, debride necrotic tissue, relieve obstruction or operate when indicated.

7. Investigations

Test	Purpose	Clinical caution
Blood cultures and source cultures	Identify organism and narrow treatment	Collect safely before antibiotics when feasible; do not delay antibiotics in shock.
Lactate/ABG or VBG	Perfusion and acid–base trend	Interpret with clinical status, seizures, liver disease and beta-agonist use.
FBC, electrolytes, renal/liver tests, glucose and coagulation	Organ dysfunction, anaemia, thrombocytopenia, dosing and DIC	Repeat to identify trajectory and treatment harm.
Urinalysis/culture, chest imaging, ultrasound or CT	Localise urinary, pulmonary, abdominal or pelvic source	Stabilise first; imaging cannot replace source control.
Malaria, VHF, dengue, HIV/TB or other targeted tests	Identify endemic or outbreak causes	Use appropriate isolation and laboratory notification.

8. Antimicrobial management

Choose empiric treatment by source, severity, community/hospital exposure, recent antibiotics, allergies, pregnancy, renal function and local resistance.
Cover likely gram-positive, gram-negative and anaerobic pathogens only as broadly as the clinical risk requires.
Use a loading dose in shock when appropriate; adjust maintenance dosing after renal/hepatic review and therapeutic monitoring.
Review cultures and clinical response daily; narrow, stop or change therapy when a non-infectious cause or resistant organism is identified.
Do not use antibiotics for every fever without infection probability; stewardship protects future patients and the individual from adverse effects.
Consider antifungal or antiviral therapy only for appropriate risk and specialist indications.

9. Fluid resuscitation

9.1 Principles

Use isotonic crystalloid as the usual first fluid for septic hypoperfusion unless a specific protocol says otherwise.
Give smaller reassessed boluses rather than an unmeasured litre after litre; use dynamic signs of responsiveness when available.
Assess lungs, oxygen requirement, jugular venous pressure/ultrasound, oedema, urine output, capillary refill, mentation and blood pressure.
Balanced crystalloids may be preferred in many adults; follow available local products and protocol.

9.2 Avoiding harm

Individualise in heart failure, kidney failure, cirrhosis, pregnancy, severe anaemia, dengue, VHF or concomitant haemorrhage.
Fluid overload causes pulmonary oedema, abdominal compartment syndrome and worse renal outcomes; reassess cumulative balance.
When hypotension persists after adequate fluid assessment, move promptly to vasopressor support rather than continuing blind fluids.

10. Vasopressors and advanced support

Norepinephrine is the recommended first-line vasopressor for adults with septic shock; titrate to a clinician-defined perfusion/MAP target.
Use a large, well-monitored peripheral vein temporarily if central access would delay treatment; inspect frequently for extravasation.
Add vasopressin in adults with inadequate pressure on escalating norepinephrine according to critical-care protocol.
Consider epinephrine or inotropy for selected refractory shock or cardiac dysfunction under ICU guidance.
Use arterial pressure monitoring, echocardiography, lung ultrasound, lactate/capillary refill trends and urine output to guide ongoing therapy.
Mechanical ventilation, renal replacement therapy, blood products and ECMO are specialist organ-support decisions.

11. Source control

Possible source	Source-control action	EMT/ward priority
Abscess/necrotising soft-tissue infection	Drainage, debridement and surgical review	Do not delay for imaging when necrotising disease is suspected.
Infected IV/urinary/vascular device	Remove or exchange when safe and send cultures	Maintain access for resuscitation; coordinate replacement.
Obstructed urinary/biliary system	Urgent drainage/stent/nephrostomy or surgery	Antibiotics alone may fail without relief of obstruction.
Peritonitis, perforation or infected obstetric tissue	Urgent surgical/obstetric intervention	Early transfer and theatre notification.
Pneumonia/meningitis	Respiratory support, cultures and targeted antimicrobial care	Isolation and airway readiness.

12. Nursing management and monitoring

Record observations at high frequency initially and trend them on one chart.
Measure urine hourly in shock; report oliguria, haematuria or sudden diuresis during recovery.
Maintain strict input/output, cumulative fluid balance and daily weight where feasible.
Assess skin, perfusion, mental status, pain, respiratory effort, lung sounds and line sites.
Administer antimicrobials on time, check cultures, allergies, renal dosing and infusion reactions.
Prevent pressure injury, delirium, aspiration, venous thromboembolism and stress-related complications.
Use aseptic line care, hand hygiene, PPE and isolation precautions for the source pathogen.
Communicate deterioration using a structured escalation tool and document response to each intervention.

13. Special populations

Children: use paediatric sepsis guidance, weight-based fluids and vasoactive support; reassess after each bolus and monitor for fluid overload.
Pregnancy/postpartum: evaluate maternal source, fetal status and obstetric causes; choose pregnancy-safe antimicrobials and involve obstetrics early.
Older adults: fever may be absent; delirium, falls and functional decline can be the presenting signs.
Renal/heart failure: use smaller fluid challenges, bedside ultrasound and earlier vasopressor/critical-care input.
Neutropenia/HIV: broaden the differential, use protective precautions where indicated and escalate empiric therapy promptly.
Malaria/VHF/dengue areas: test and isolate appropriately; fluid strategy may differ from routine bacterial sepsis.

14. Complications

Complication	Clues	Response
ARDS/respiratory failure	Increasing oxygen need, crackles, work of breathing or low SpO₂	Oxygen, lung-protective ventilation/critical care and fluid review.
Acute kidney injury	Oliguria, rising creatinine, hyperkalaemia or acidosis	Perfusion/source management, avoid nephrotoxins, renal review/RRT.
DIC/bleeding	Purpura, oozing lines, falling platelets/fibrinogen	Source control, labs, blood components only for clinical indications.
Encephalopathy/seizures	Confusion, reduced GCS or convulsions	Glucose, oxygen, seizure treatment and neurological review.
Fluid overload	Oedema, pulmonary crackles, weight gain, worsening oxygenation	Stop unnecessary fluids, reassess perfusion and consider diuresis/RRT when stable.

15. Prevention and antimicrobial stewardship

Hand hygiene, safe injections, device bundles, wound care, vaccination and early treatment of localized infection prevent sepsis.
Use sterile technique for lines and catheters; remove devices as soon as no longer needed.
Educate patients to seek care for confusion, fast breathing, severe pain, cold skin, low urine or worsening infection.
Audit time-to-antibiotic, culture quality, source-control delays, fluid overload and de-escalation.
Follow infection-prevention precautions for meningitis, VHF, respiratory or gastrointestinal sources.

16. Handover and transfer

State “suspected septic shock” early and report source, onset and response to treatment.
Give serial vital signs, lactate, urine output, mental status, oxygen/ventilation, fluids, antimicrobials, vasopressor dose and access site.
Tell the receiving team about allergies, pregnancy, renal/heart disease, resistant organisms and pending cultures.
Transfer with pumps, oxygen, monitoring, emergency drugs and an escort trained to manage deterioration.

17. Clinical scenarios

Scenario 1 – Pneumonia and shock. A patient has fever, RR 34/min, SpO₂ 86%, confusion, BP 82/48 and crackles. The EMT gives oxygen, obtains glucose/IV access, calls the sepsis team, obtains cultures without delaying broad empiric antibiotics, gives reassessed crystalloid, prepares norepinephrine/critical care when hypotension persists and arranges monitored transfer.

Scenario 2 – Obstructed urinary sepsis. A patient with fever, flank pain, oliguria and hypotension has hydronephrosis. Antibiotics are started, but the team also alerts urology because drainage is source control; repeated fluids alone will not resolve the obstruction.

Scenario 3 – Fluid overload. A patient with heart failure remains hypotensive after a small bolus but becomes breathless with crackles. The team stops blind fluid loading, gives oxygen, calls critical care, assesses cardiac function and starts vasopressor support when indicated.

18. Common errors

Waiting for a positive culture before treating high-probability shock.
Using qSOFA or one blood-pressure reading as the only screen.
Giving litres of fluid without reassessment or ignoring heart/renal failure.
Delaying vasopressors while repeatedly attempting central access.
Forgetting source control, device removal or surgical referral.
Failing to review/narrow antibiotics when cultures return.
Ignoring post-sepsis weakness, cognitive symptoms and rehabilitation.

19. Quick revision questions

Define sepsis and septic shock.
List six early signs of occult hypoperfusion.
What are the priorities in the first hour?
When should cultures be collected?
Why must antibiotics not be delayed in shock?
What is the usual first-line adult vasopressor?
How do you decide whether more fluid is safe?
Give five examples of source control.
What should the nurse monitor hourly in septic shock?
List five prevention and stewardship measures.

20. Key takeaways

References and further reading

Septic Shock: Recognition, Resuscitation and Definitive Management Read More »

Encephalitis: Recognition, Emergency Management and Nursing Care

Why encephalitis is an emergency. Encephalitis is inflammation of brain tissue that can progress from fever and headache to seizures, coma, respiratory failure, raised intracranial pressure and permanent neurological disability. Viral, bacterial, parasitic, fungal, autoimmune and post-infectious causes can look similar at first. The EMT must protect the airway, check glucose, stop seizures, recognise meningitis/encephalitis, arrange urgent hospital care and avoid delays for a complete diagnostic work-up.

1. Learning objectives

Define encephalitis and distinguish it from meningitis, encephalopathy and seizure-related confusion.
Recognise common infectious, autoimmune, toxic and metabolic causes.
Perform a safe ABCDE and neurological assessment, including glucose and seizure status.
Identify raised intracranial pressure, impending herniation and respiratory failure.
Explain urgent testing, lumbar-puncture precautions, empiric therapy and supportive care.
Plan nursing monitoring, rehabilitation, infection prevention and family education.

2. Definition and pathophysiology

Encephalitis is inflammation of the brain parenchyma causing neurological dysfunction. Meningoencephalitis affects both brain tissue and meninges. Encephalopathy is broader brain dysfunction from systemic or metabolic causes and may occur without inflammation. Brain swelling, inflammatory injury, seizures, impaired consciousness and disruption of cerebral perfusion can cause secondary neuronal damage.

In Uganda and other tropical settings, the differential includes herpes simplex virus, varicella-zoster, arboviruses, enteroviruses, measles, HIV-related infections, bacterial meningitis with brain involvement, cerebral malaria, tuberculosis, cryptococcosis, autoimmune encephalitis, toxins, hypoglycaemia, electrolyte disturbance and post-infectious disease.

Do not wait for classic neck stiffness. A patient with fever plus new confusion, personality change, seizure, focal deficit or reduced consciousness needs urgent evaluation even when the neck is supple.

3. Causes and clinical clues

Cause/group	Clues	Emergency implications
HSV-1/HSV-2 encephalitis	Fever, headache, confusion, seizures, personality/language change, focal deficits; temporal-lobe features	Empiric IV acyclovir is time-critical when suspected, with renal monitoring.
VZV and other viruses	Rash, cranial neuropathy, ataxia, immunosuppression or recent viral illness	Isolation when indicated and specialist antiviral pathway.
Arboviral encephalitis	Seasonal/vector exposure, fever, tremor, weakness, movement disorder or flaccid paralysis	Supportive critical care and vector/public-health notification.
Bacterial meningoencephalitis	Fever, meningism, shock, purpura, rapid deterioration or focal infection	Immediate empiric antibacterial therapy; droplet precautions for suspected meningococcal disease.
Cerebral malaria	Endemic exposure, coma, seizures, hypoglycaemia, anaemia or jaundice	Urgent malaria testing and parenteral antimalarial pathway.
TB/fungal/parasitic disease	Subacute illness, weight loss, HIV/immunosuppression, cranial neuropathies	Specialist testing and prolonged therapy; raised ICP may make LP unsafe.
Autoimmune/paraneoplastic encephalitis	Psychiatric change, memory loss, dyskinesia, autonomic instability or seizures without infection source	Exclude infection first; specialist immunotherapy and seizure management.
Toxic/metabolic encephalopathy	Hypoglycaemia, sodium abnormality, poisoning, liver/renal failure, heat illness or drug effect	Correct reversible cause while continuing neurological assessment.

4. Recognition and red flags

Urgent resuscitation/red flags: GCS falling, repeated or ongoing seizure, focal weakness, unequal pupils, papilloedema, Cushing response, severe headache with vomiting, abnormal posturing, respiratory irregularity, hypoxia, shock, hypoglycaemia, purpura, pregnancy, immunocompromise, recent neurosurgery or a rapidly progressive course.

Fever or recent infection plus altered mental status is a high-risk combination.
Seizures may be subtle: eye deviation, facial twitching, automatisms, unexplained agitation or failure to regain baseline consciousness.
Normal blood pressure or temperature does not exclude severe intracranial disease.

5. History taking

Time and sequence of fever, headache, vomiting, confusion, behaviour change, seizures and focal weakness.
Witness description: onset, duration, movements, eye position, cyanosis, incontinence, injury and recovery after a seizure.
Recent infections, rash, ear/sinus infection, animal/mosquito/tick exposure, travel, vaccines and sick contacts.
HIV status, TB exposure, immunosuppression, cancer, pregnancy and recent medications or toxins.
Diabetes, renal/liver disease, epilepsy, sickle cell disease, malaria exposure and antimalarial use.
Recent neurosurgery, head trauma, lumbar puncture, injection drug use or invasive procedure.

6. ABCDE and neurological assessment

A – Airway

Assess gag/cough, secretions, vomiting, tongue obstruction and aspiration. Use jaw thrust/positioning, suction and airway adjuncts as trained; prepare an experienced airway team for GCS decline.

B – Breathing

Check respiratory rate, SpO₂, effort and pattern. Central hypoventilation, aspiration, seizures or raised ICP can cause respiratory failure; give oxygen for hypoxaemia.

C – Circulation

Check pulse, blood pressure, capillary refill, temperature and urine output. Treat shock cautiously with isotonic fluid and investigate sepsis, bleeding and dehydration.
Obtain IV access and blood samples only when safe; do not delay time-critical therapy.

D – Disability

Record GCS/AVPU, pupils, limb power, speech, facial symmetry, sensation and glucose. Repeat after seizure treatment or any deterioration.

E – Exposure

Look for rash, petechiae, trauma, needle marks, ear/mastoid infection, shingles, bites and signs of systemic infection while protecting dignity and warmth.

7. Seizure and airway emergencies

Protect from injury, clear nearby objects and time the seizure; do not restrain or put anything in the mouth.
Place in a safe lateral position when possible, suction secretions with PPE and give oxygen.
Check glucose as soon as feasible and treat hypoglycaemia under protocol.
For ongoing convulsive status, give a protocol-selected benzodiazepine and escalate for second-line therapy/airway support.
After the seizure, reassess GCS, pupils, breathing, temperature, glucose, focal signs and injuries.
Persistent coma after a seizure is not automatically “post-ictal”; consider ongoing non-convulsive seizure, encephalitis, malaria, hypoxia, toxic/metabolic causes or raised ICP.

8. Raised intracranial pressure and herniation

Warning signs include deteriorating consciousness, repeated vomiting, worsening headache, unequal or sluggish pupils, new focal deficit, abnormal posturing, bradycardia with hypertension and irregular breathing.
Keep the head midline and elevate about 30 degrees if perfusion permits; avoid neck compression, hypoxia, hypotension, fever and unnecessary stimulation.
Maintain oxygenation and normoglycaemia; treat seizures promptly.
Urgently involve anaesthesia/critical care/neurosurgery. Do not perform lumbar puncture when there are signs of mass effect, severe reduced consciousness, focal deficit, papilloedema, uncontrolled seizure or cardiorespiratory instability until senior review.
Hyperventilation is not routine; use only as a temporary specialist-directed rescue for impending herniation.

9. Investigations and lumbar-puncture safety

Test	Purpose	Safety/interpretation
Glucose, FBC, electrolytes, renal/liver tests, malaria test	Find reversible/metabolic causes, cerebral malaria and organ dysfunction	Correct abnormalities promptly; a negative malaria test does not exclude encephalitis.
Blood cultures	Identify bacterial, fungal or bloodstream infection	Collect before antibiotics only if it will not delay treatment.
CT/MRI brain	Mass lesion, oedema, haemorrhage, stroke, abscess or temporal-lobe changes	Imaging does not replace empiric therapy; stabilise first.
Lumbar puncture and CSF	Cells, protein, glucose, Gram stain/culture, PCR and targeted tests	Perform promptly when safe; defer for raised ICP, unstable airway/breathing/circulation, focal mass-effect signs or severe coagulopathy.
EEG	Non-convulsive seizures, encephalopathy pattern and prognosis	Do not delay treatment of clinical status epilepticus while waiting.
Targeted PCR/serology	HSV/VZV, arbovirus, HIV, TB, autoimmune and other causes	Choose tests by epidemiology, syndrome and specialist advice.

10. Immediate hospital management

Admit to a monitored area; use isolation precautions appropriate to the suspected pathogen.
Stabilise airway, breathing and circulation; avoid hypoxia, hypotension, hypoglycaemia and hyperthermia.
Start empiric IV acyclovir promptly when HSV encephalitis is clinically suspected, with renal-dose and hydration monitoring; do not wait for CSF PCR.
If bacterial meningitis/meningoencephalitis is possible, give empiric IV antibacterial therapy and corticosteroid according to local/WHO protocol, ideally after blood cultures and LP only when safe.
Treat severe malaria immediately through the parenteral artesunate pathway when indicated.
Manage seizures, electrolyte abnormalities, fever, pain, agitation and aspiration risk.
Consult infectious diseases, neurology, critical care, paediatrics/obstetrics and public health as appropriate.

11. Supportive and critical-care management

Use continuous pulse oximetry and frequent neurological observations; document GCS and pupil trend.
Provide enteral nutrition when airway is protected; manage aspiration and pressure-injury risk.
Use isotonic fluids for shock or dehydration but avoid fluid overload in raised ICP, renal failure or cardiac disease.
Control fever with paracetamol and safe environmental measures; investigate the cause rather than masking deterioration.
Prevent venous thromboembolism and stress ulcers according to critical-care protocol, balancing bleeding risk.
Monitor sodium closely; rapid correction of severe dysnatremia can worsen neurological injury.
Escalate for invasive ventilation, vasopressor support, intracranial-pressure management or transfer to ICU.

12. Nursing care plan

Problem	Interventions	Outcome/alert
Reduced consciousness/airway risk	Side positioning, suction, airway observations, aspiration precautions, GCS/pupil checks	Airway protected; immediate escalation for falling GCS or irregular breathing
Seizure risk	Padded surroundings, oxygen/suction ready, seizure chart, medication timing and recovery assessment	Seizure stops and patient returns toward baseline
Raised ICP	Head midline/elevated, quiet environment, prevent hypoxia/hypotension/fever, frequent neuro observations	No new pupil asymmetry, posturing or deterioration
Infection transmission	Hand hygiene, droplet/contact precautions when indicated, safe specimen and waste handling	No staff or patient cross-infection
Immobility/nutrition	Pressure-area care, passive movement, feeding/swallow review and fluid balance	Skin intact, adequate nutrition and no aspiration
Family distress	Simple explanations, updates, consent/confidentiality and rehabilitation planning	Family understands warning signs and follow-up

13. Infection prevention and public-health issues

Use droplet precautions for suspected meningococcal disease until the appropriate period after effective antibiotics; use pathogen-specific precautions for VHF, measles, varicella or other transmissible causes.
Use standard precautions for blood, CSF, vomit, urine and respiratory secretions; handle sharps safely.
Notify public health for suspected vaccine-preventable disease, VHF, meningococcal clusters or unusual encephalitis.
Consider mosquito/tick control and vaccination advice where arboviral or vaccine-preventable causes are suspected.

14. Recovery, rehabilitation and prevention

Assess memory, speech, swallowing, mood, behaviour, movement, hearing and vision before discharge.
Arrange physiotherapy, occupational therapy, speech/swallow therapy, neuropsychology and seizure follow-up as needed.
Teach family seizure first aid, medication adherence, driving/work restrictions and return precautions.
Complete vaccination, mosquito protection, HIV/TB care and exposure prevention according to the cause.
Monitor for post-encephalitic epilepsy, cognitive impairment, fatigue, depression, sleep disturbance and focal deficits.

15. Clinical scenarios

Scenario 1 – Fever and confusion. A 24-year-old develops fever, personality change, aphasia and a focal seizure. The EMT protects the airway, gives oxygen, checks glucose, treats the seizure under protocol, obtains urgent IV access and alerts the clinician that HSV encephalitis is possible. CT/LP and empiric therapy are organised in parallel; acyclovir is not delayed while waiting for CSF.

Scenario 2 – Suspected meningitis with shock. A patient has fever, neck stiffness, purpuric rash, hypotension and confusion. The team uses droplet precautions, ABCDE resuscitation, blood cultures, urgent empiric antibacterial therapy and senior/critical-care referral. Lumbar puncture is deferred until the patient is stable and contraindications are reviewed.

Scenario 3 – Post-seizure coma. A child remains unresponsive 20 minutes after a seizure. The EMT rechecks glucose, oxygenation, temperature, pupils and seizure activity rather than assuming a normal post-ictal state. Persistent non-convulsive status, cerebral malaria, meningitis and raised ICP remain possible.

16. Common errors

Waiting for neck stiffness before considering encephalitis.
Calling persistent coma “post-ictal” without checking glucose and ongoing seizures.
Delaying acyclovir or antibiotics for imaging/LP when clinical suspicion is high.
Performing LP in a patient with raised ICP, shock, severe coagulopathy or a deteriorating airway.
Ignoring cerebral malaria and hypoglycaemia in endemic settings.
Giving excessive fluids or allowing fever, hypoxia, hypotension and hyponatraemia to persist.
Failing to plan rehabilitation and family education after survival.

17. Quick revision questions

What clinical features make encephalitis likely?
List four infectious and three non-infectious causes.
What are the first actions during an active seizure?
When should lumbar puncture be deferred?
Why is empiric acyclovir time-critical?
How can cerebral malaria be distinguished and treated urgently?
What findings suggest raised ICP or impending herniation?
Which observations should nursing staff trend?
When are droplet or other transmission-based precautions needed?
What rehabilitation needs must be assessed before discharge?

18. Key takeaways

BRAIN SAFE:
Breathing and airway first | Recognise fever plus altered mentation | Antivirals/antibiotics early when indicated | Investigate glucose, malaria, CSF and imaging safely
Seizures treated and timed | Avoid unsafe LP | Fight hypoxia, hypotension and fever | Escalate to critical care and rehabilitation

References and further reading

Encephalitis: Recognition, Emergency Management and Nursing Care Read More »

Skin and Soft-Tissue Infections: Emergency Assessment and Management

Why this topic matters. A red, swollen or painful area may be minor cellulitis, but it can also be the first visible sign of sepsis, necrotising fasciitis, diabetic foot infection, toxic shock, an infected bite or a deep-space infection. EMTs must examine the whole patient, compare the local findings with systemic physiology and identify when antibiotics alone are unsafe because drainage or urgent surgery is required. Drug selection and duration must follow the Uganda Clinical Guidelines, local antibiogram, allergy history, renal function and senior clinician prescription.

1. Learning objectives

Define common skin and soft-tissue infections (SSTIs) and describe the skin barrier and routes of infection.
Differentiate cellulitis, erysipelas, abscess, infected wound, diabetic foot infection and necrotising infection.
Recognise sepsis, toxic shock, deep-space infection and necrotising fasciitis early.
Perform focused history, examination, severity assessment and safe investigations.
Explain first aid, wound care, source control, antimicrobial principles and surgical referral.
Plan nursing interventions, monitoring, prevention, patient education and discharge safety-netting.

2. What is an SSTI?

Skin and soft-tissue infections involve the epidermis, dermis, subcutaneous tissue, fascia, muscle or structures around a wound. They range from superficial impetigo and infected abrasions to abscesses, cellulitis, infected ulcers, diabetic foot infection and rapidly fatal necrotising fasciitis. Common organisms include Staphylococcus aureus, beta-haemolytic streptococci, mixed aerobic/anaerobic flora in chronic wounds, and water/animal-associated organisms after special exposures.

Infection enters through cuts, ulcers, burns, injections, surgery, bites, fungal fissures, oedema or an impaired immune barrier. Diabetes, peripheral vascular disease, lymphoedema, malnutrition, HIV, sickle-cell disease, obesity, immunosuppression and delayed presentation increase risk.

3. Classification and clinical patterns

Condition	Typical findings	Emergency concern
Impetigo/ecthyma	Superficial erosions, honey-coloured crusts or deeper punched-out ulcers	Spread, dehydration in children, post-streptococcal complications or extensive disease.
Folliculitis/furuncle/carbuncle	Pustule or tender boil centred on a hair follicle; carbuncle has multiple draining points	Abscess requiring drainage, diabetes, recurrent MRSA or systemic toxicity.
Cellulitis	Diffuse erythema, warmth, swelling and tenderness without a drainable collection	Rapid progression, lymphangitis, sepsis, facial/orbital involvement or treatment failure.
Erysipelas	Raised, sharply demarcated bright-red plaque, often with fever	Bacteraemia, facial involvement and rapid systemic deterioration.
Abscess	Localised painful, fluctuant or indurated collection, sometimes with a central point	Source control needed; deep, perianal, hand, breast, face or neck sites need specialist review.
Infected wound/ulcer/diabetic foot	Purulent drainage, malodour, increasing pain, necrotic tissue or surrounding cellulitis	Deep infection, osteomyelitis, ischaemia, amputation risk and sepsis.
Necrotising fasciitis	Rapidly worsening pain/swelling, systemic toxicity, bullae, skin anaesthesia, crepitus or necrosis	Immediate surgical emergency; do not wait for imaging or antibiotic response.

4. Triage and red flags

Send to resuscitation/urgent senior review: shock, confusion, severe pain out of proportion, rapidly spreading erythema, bullae, skin discoloration or necrosis, crepitus, severe systemic toxicity, high fever or hypothermia, tachypnoea, facial/orbital or neck swelling, perineal infection, hand infection, immunosuppression, diabetes with a foot wound, exposed tendon/bone, vascular compromise, inability to walk/use the limb or failed outpatient treatment.

Mark the edge of erythema with date/time and measure length, width and circumference.
Record pulse, blood pressure, respiratory rate, SpO₂, temperature, mental status, glucose and urine output.
Ask how fast the lesion has changed; hours rather than days strongly increases concern.

5. History taking

5.1 Lesion history

Onset, speed of spread, pain severity and pain out of proportion to appearance.
Trauma, puncture, injection, surgery, burn, ulcer, bite, tattoo, piercing or water exposure.
Purulent discharge, odour, blisters, numbness, colour change and loss of function.
Previous SSTI, abscess, resistant organisms or recent antibiotics/hospitalisation.

5.2 Host and exposure risks

Diabetes, HIV, sickle-cell disease, vascular disease, lymphoedema, malnutrition and immunosuppressive medicines.
Animal/human bite, freshwater/seawater, soil, farm or flood exposure.
Recent travel, crowding, contact sports, shared razors/towels or household boils.
Drug allergy, renal/liver disease, pregnancy, anticoagulants and tetanus-immunisation status.

6. Focused examination

General: toxic appearance, fever/hypothermia, hydration, mental status and sepsis physiology.
Inspect: site, size, colour, border, crust, ulcer, bullae, necrosis, discharge, lymphangitis and satellite lesions.
Palpate gently: warmth, tenderness, induration, fluctuance, crepitus and sensation. Do not repeatedly squeeze a lesion.
Function: range of motion, tendon/nerve function, distal pulses, capillary refill and limb compartment signs.
Search for a source: interdigital fungal infection, pressure area, IV site, diabetic ulcer, surgical wound, bite, abscess or foreign body.
Compare sides: limb circumference, temperature, sensation, pulses and progression from the last mark.

7. Differentiating cellulitis, abscess and necrotising infection

Feature	Cellulitis	Abscess	Necrotising fasciitis
Distribution	Diffuse, spreading erythema	Localised collection	Rapidly expanding, often beyond visible skin changes
Pain	Tender and proportional	Focal throbbing/tenderness	Severe or out of proportion; later anaesthesia may occur
Palpation	Warm, indurated, no clear fluctuance	Fluctuant or indurated centre	Woody induration, crepitus or tense oedema
Skin	Red and warm	Pointing, pustule or drainage	Bullae, dusky colour, ecchymosis, skin slough or necrosis
Systemic illness	May be mild or severe	Usually local unless extensive	Often toxic, hypotensive, confused or rapidly deteriorating
Definitive action	Antibiotic plan and elevation/follow-up	Incision and drainage when indicated	Immediate surgical exploration/debridement plus broad empiric therapy

8. First aid and pre-hospital care

Use hand hygiene, gloves and eye protection if blood, pus or splash is possible.
Control bleeding with direct pressure; do not pack an abscess blindly or close a dirty wound.
Cover open wounds with a sterile/non-adherent dressing; do not apply household chemicals, ash, soil, toothpaste or unprescribed antibiotics.
Elevate an infected limb when it does not worsen pain or perfusion and remove constrictive jewellery/clothing.
Check glucose in a diabetic or systemically unwell patient; give oxygen for hypoxaemia.
For suspected sepsis or necrotising infection, obtain rapid transport after calling the receiving hospital; do not delay for extensive wound cleaning.
For bites, irrigate/clean promptly, assess tetanus and rabies risk, and transfer for bite-specific management.

9. Investigations

Investigation	Use	Limitations/safety
Glucose, FBC, renal/liver function and lactate	Severity, sepsis, diabetes, organ injury and antibiotic dosing	Normal results do not exclude early necrotising infection.
Wound/pus culture and susceptibility	Guide therapy in purulent, recurrent, severe or treatment-failure infection	Obtain deep material when possible; superficial swabs may reflect colonisation.
Blood cultures	Bacteraemia, sepsis, severe cellulitis or immunocompromise	Collect safely, ideally before antibiotics if this does not delay treatment.
Ultrasound	Detect a drainable abscess or fluid collection	A negative scan does not rule out deep necrotising disease.
X-ray/CT/MRI	Gas, foreign body, deep extension, osteomyelitis or complex anatomy	Never delay emergency surgical review for imaging when necrotising infection is likely.
Probe-to-bone/vascular assessment	Diabetic foot depth, ischaemia and osteomyelitis risk	Use trained clinicians and involve surgery/vascular teams early.

10. Antimicrobial and medical management principles

Use local guidelines and the likely organism, anatomic site, severity, allergies, pregnancy, renal function and resistance pattern to choose antibiotics.
Non-purulent uncomplicated cellulitis usually needs streptococcal/MSSA-active therapy; purulent infection requires assessment for drainage and possible staphylococcal/MRSA coverage according to local data.
Severe infection, immunocompromise, perineal infection, bites, water exposure, diabetic foot infection and necrotising disease require broader specialist-directed coverage.
Take cultures when severe, recurrent, unusual, immunocompromised or not responding; narrow therapy when results permit.
Give antibiotics promptly for sepsis or suspected necrotising infection, but do not let antibiotics replace source control.
Adjust dose and interval for renal/hepatic impairment and review IV-to-oral switch daily.
Provide analgesia, glucose control, hydration and tetanus prophylaxis as indicated.

11. Abscess and source control

Assess location, depth, neurovascular status and proximity to face, hand, breast, anus, genitals, tendon or joint.
Use ultrasound or surgical review for deep/uncertain collections.
Incision and drainage is the key treatment for a drainable abscess; antibiotics alone may fail when pus remains enclosed.
Use aseptic technique, analgesia/local anaesthesia and sharps safety; send appropriate material for culture in severe/recurrent cases.
Pack or leave the wound open only when clinically indicated; arrange dressing review and clear instructions.
Facial, hand, deep neck, perirectal, breast, genital and joint-adjacent abscesses need early specialist involvement.

12. Necrotising fasciitis and toxic shock

Do not wait for skin necrosis. Severe pain out of proportion, rapidly progressive swelling, systemic toxicity, bullae, crepitus, skin anaesthesia or a tense woody limb should trigger immediate surgical consultation and resuscitation.

ABCDE, oxygen, glucose, IV access, blood tests/cultures and cautious fluid resuscitation.
Urgent surgical exploration and serial debridement are definitive; imaging must not create a dangerous delay.
Start broad empiric IV antibiotics covering streptococci, staphylococci, gram-negative organisms and anaerobes according to local protocol.
Consider toxin-suppressing therapy and IV immunoglobulin only on specialist advice.
Monitor for septic shock, acute kidney injury, rhabdomyolysis, coagulopathy, respiratory failure and limb loss.

13. Special SSTIs

13.1 Diabetic foot and chronic ulcers

Inspect footwear, pressure points, pulses, sensation, depth, odour and exposed tendon/bone.
Check glucose and vascular status; off-load pressure and avoid walking on a threatened foot.
Coordinate wound care, debridement, imaging, culture and diabetes/vascular/podiatry review.

13.2 Animal and human bites

Wash/irrigate promptly, assess tendon, nerve, vessel and joint injury, and document the animal and time.
Consider rabies post-exposure prophylaxis, tetanus and bite-specific antimicrobial therapy under national guidance.
Hand, face, genital, puncture, immunocompromised and delayed presentations need urgent review.

13.3 Periorbital, facial and neck infection

Assess vision, eye movement, proptosis, severe headache, trismus, dysphagia, drooling and airway compromise.
Urgent ophthalmology/ENT/maxillofacial review is required for orbital or deep-neck signs.

14. Nursing interventions and monitoring

Priority	Interventions	Escalate when
Sepsis/perfusion	Serial vital signs, mental status, glucose, urine output, lactate and fluid response	Hypotension, rising respiratory rate, confusion, oliguria or increasing lactate
Wound	Measure/mark erythema, assess pain, colour, drainage, odour, pulses and sensation; aseptic dressings	Rapid spread, new bullae, necrosis, disproportionate pain or neurovascular change
Antibiotic safety	Check allergy, renal function, timing, route, cultures and adverse effects; review IV need daily	Rash, anaphylaxis, diarrhoea, renal deterioration or treatment failure
Mobility/pressure	Elevate limb when appropriate, off-load diabetic foot, prevent pressure injury and falls	Increasing pain, compartment signs, inability to mobilise or ischaemia
Education	Hand hygiene, wound care, medicine adherence, no squeezing, return precautions and household hygiene	Caregiver cannot perform dressing or patient lacks follow-up access

15. Prevention

Clean and cover cuts, promptly irrigate wounds and seek care for increasing redness, pain, swelling or fever.
Manage diabetes, oedema, fungal foot disease and vascular problems; inspect feet daily.
Do not share razors, towels, needles or personal wound equipment.
Use hand hygiene, clean injection technique and appropriate PPE in healthcare settings.
Complete tetanus vaccination and follow bite/rabies prevention guidance.
Use antibiotics only when indicated and complete prescribed courses; never save or share them.

16. Discharge and referral

Outpatient care is appropriate only for a stable patient with a superficial/localised infection, reliable oral intake, no danger sign, a clear antibiotic/wound plan and accessible review.

Return immediately for fever, confusion, fainting, fast breathing, spreading redness, severe/worsening pain, bullae, black skin, reduced urine, vomiting or inability to take medicines.
Keep dressings clean and dry, wash hands before/after care and do not squeeze or lance lesions at home.
Return for wound review, dressing change, culture result, suture removal or IV-to-oral antibiotic review.
Admit or refer for sepsis, necrotising infection, deep abscess, facial/hand/perineal infection, diabetic foot, immunosuppression, failed outpatient therapy or poor follow-up support.

17. Clinical scenarios

Scenario 1 – Cellulitis. A patient has a warm, tender lower-leg plaque, stable observations and no fluctuance. The EMT marks the edge, checks diabetes and pulses, cleans the entry wound, elevates the leg and arranges clinician assessment for local antibiotic therapy and follow-up. The patient receives return precautions if the redness spreads or systemic symptoms develop.

Scenario 2 – Abscess. A painful fluctuant axillary swelling has no shock. The team avoids squeezing it in triage, gives analgesia, assesses for diabetes/immunosuppression and arranges aseptic incision and drainage, culture when indicated, wound review and antibiotic decision based on severity and local guidance.

Scenario 3 – Necrotising infection. A diabetic patient has severe thigh pain, fever, tachycardia and dusky bullae after a minor cut. The EMT treats this as a surgical emergency: resuscitation, glucose, IV access, cultures if they do not delay care, broad protocol antibiotics, urgent surgical call and rapid theatre transfer. No time is lost waiting for a scan or the skin to turn black.

18. Common errors

Calling rapidly progressive pain “simple cellulitis.”
Using topical creams or antibiotics alone for a drainable abscess.
Delaying surgery for imaging in suspected necrotising fasciitis.
Failing to assess pulses, sensation, tendon function and compartment signs.
Ignoring diabetes, HIV, malnutrition, oedema or vascular disease.
Closing a contaminated/infected wound without a source-control plan.
Giving antibiotics without allergy/renal review or microbiology follow-up.
Discharging without marking progression, review date and safety-net advice.

19. Quick revision questions

What is the difference between cellulitis, erysipelas and an abscess?
List six red flags for necrotising fasciitis.
Why is source control important?
Which SSTI sites require especially early specialist review?
What tests help assess severe or recurrent infection?
What are the first actions for a human or animal bite?
How should a diabetic foot infection be assessed?
When are antibiotics alone inadequate?
What should be monitored during IV antibiotics?
Write five discharge return precautions.

20. Key takeaways

References and further reading

Skin and Soft-Tissue Infections: Emergency Assessment and Management Read More »