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Communication Essentials for Emergency Medicine and Health-Care Practice

Why this matters to emergency medicine students: Communication is a clinical skill, a patient-safety intervention and a professional responsibility. A technically correct treatment can still fail when the patient does not understand it, the handover omits a warning sign, the team does not close the communication loop or a language barrier is ignored. Effective health communication should be accessible, actionable, credible, relevant, timely and understandable; it also has to respect dignity, culture, privacy, consent and health literacy.

Learning objectives

Define communication and describe its purpose in personal, clinical, emergency and public-health settings.
Explain the communication process, modes, channels, principles and feedback loop.
Apply soft skills such as empathy, respect, assertiveness, teamwork, adaptability and emotional control.
Recognise physical, psychological, semantic, cultural, organisational and technological barriers.
Use patient-centred, culturally safe, trauma-informed and health-literacy-sensitive communication.
Apply structured communication such as SBAR, closed-loop communication and read-back during emergencies.
Communicate ethically while protecting privacy, confidentiality, consent and professional boundaries.
Evaluate communication quality and develop a personal improvement plan.

Definition of communication

Communication is the deliberate or unintended exchange of information, ideas, feelings, instructions and meaning between people or groups. It includes what is said, how it is said, what is written or displayed, what the body expresses and what the receiver understands. Communication is successful only when the intended meaning is reasonably understood and can guide an appropriate response.

In emergency medicine, communication occurs between the patient, relatives, bystanders, dispatcher, EMT, nurse, doctor, driver, receiving facility, laboratory, pharmacy and community agencies. Each link can preserve or distort the message. A clear message protects the patient; a vague message can delay airway support, medication, transport or escalation.

Why communication is important in health care

Assessment: history, symptoms, concerns, medication use, allergies and social circumstances are discovered through communication.
Trust and cooperation: respectful explanations reduce fear and improve participation in examination, treatment and referral.
Patient safety: accurate orders, read-back, handover and escalation reduce omissions and preventable errors. Communication failures are recognised contributors to patient-safety incidents.
Continuity of care: the next team can continue treatment when information is timely, complete and organised.
Health education: patients can understand prevention, medicines, warning signs and follow-up.
Team performance: shared mental models, psychological safety and respectful challenge support coordinated action.
Professional accountability: contemporaneous records show what was assessed, explained, agreed and handed over.

The communication process

Communication is a dynamic process rather than a one-way transfer of words. The sender forms an intention, encodes it into a message, selects a channel, sends it through a context, and the receiver decodes it. Feedback demonstrates whether the message was understood. Noise can interfere at every stage.

Sender: identifies the purpose, audience, urgency and desired action.
Encoding: translates thoughts into words, symbols, gestures, tone, diagrams or written text.
Message: the actual content, including facts, feelings, instructions and non-verbal cues.
Channel: face-to-face speech, telephone, radio, written note, electronic record, email, text, image or public announcement.
Receiver: pays attention, interprets the message and considers the context.
Decoding: gives meaning to the message using language, culture, previous knowledge and emotion.
Feedback: questions, teach-back, read-back, a task being repeated or a change in behaviour confirms understanding.
Noise: anything that distorts the message—sirens, pain, fear, jargon, poor network, fatigue, assumptions or competing priorities.

MESSAGE — Make the purpose clear; Express simply; Select the right channel; Seek feedback; Acknowledge emotion; Guard privacy; Escalate when needed.

Modes of communication

Mode	Examples	Strengths	Risks
Verbal/oral	Conversation, briefing, telephone, radio, teaching and handover.	Fast, interactive and allows immediate questions.	Noise, accent, stress, memory loss and misheard numbers.
Non-verbal	Facial expression, eye contact, posture, gesture, touch, distance and silence.	Conveys emotion, attention, confidence and respect.	Cultural misinterpretation, mixed signals and unconscious bias.
Written	Clinical notes, consent forms, referral letters, reports, discharge instructions and emails.	Creates a durable record and supports continuity.	Illegibility, missing context, jargon, delayed reading and privacy breaches.
Visual	Pictures, charts, maps, symbols, demonstration and video.	Supports low literacy, memory and complex explanations.	Ambiguous symbols, inaccessible colour choices or misleading scale.
Electronic/digital	EMR, SMS, telehealth, messaging, e-prescribing and electronic referral.	Rapid sharing, searchable history and remote collaboration.	Wrong recipient, cyber-risk, poor connectivity, copy-forward errors and downtime.

The principles of effective communication

The 7 Cs

Clear: use plain language and one main idea at a time.
Concise: remove unnecessary words without omitting safety-critical detail.
Complete: provide the information needed for the receiver to act safely.
Correct: verify names, doses, times, numbers, facts and spelling.
Concrete: use specific observations rather than vague labels such as “looks bad.”
Courteous: communicate with dignity, patience and respect even under pressure.
Considerate: adapt to the receiver’s language, culture, disability, health literacy and emotional state.

Additional clinical principles

Identify yourself and your role; confirm the patient’s identity using approved identifiers.
Explain why you need information or permission, and check consent before sensitive questions or examination.
Use the least threatening, most appropriate environment possible; protect privacy and confidentiality.
Listen before correcting, acknowledge feelings and avoid premature judgement.
Share uncertainty honestly and state what will happen next.
Use feedback, teach-back, read-back and closed-loop communication for safety-critical messages.
Document significant communication, refusals, advice, escalation and agreed plans.

Communication in the emergency encounter

Prepare: check scene safety, PPE, role, urgency and available interpreter or communication aid.
Open: greet, identify yourself, confirm the patient and establish immediate concern.
Stabilise while speaking: do not postpone life-saving ABCDE actions for a long conversation.
Orient: explain what you are doing—“I am checking your breathing and pulse because you are short of breath.”
Gather: ask focused questions, allow the patient to speak, clarify contradictions and include a trusted support person with consent.
Explain: state findings, likely next steps, benefits, risks and alternatives in understandable language.
Confirm: ask the patient to repeat key instructions or demonstrate them.
Close: provide warning signs, follow-up, contact information and an opportunity for questions.

Soft skills for the EMT and health worker

Soft skill	Observable behaviour	Clinical value
Empathy	Name the emotion and show that the person’s experience matters.	Builds trust and improves disclosure.
Respect	Use preferred name, protect dignity and avoid humiliating language.	Supports consent and cooperation.
Assertiveness	State a concern directly, respectfully and with evidence.	Enables escalation when a patient deteriorates.
Adaptability	Change pace, language, channel or aid for the situation.	Works across cultures, disabilities and emergencies.
Emotional regulation	Pause, breathe, control tone and remain task-focused.	Prevents panic and aggressive exchanges.
Teamwork	Share information, invite input and clarify roles.	Creates a shared mental model.
Conflict management	Address the issue, not the person; seek common goals.	Protects relationships and patient safety.
Reliability	Return calls, complete handovers and document agreed actions.	Prevents tasks disappearing between teams.

Patient-centred communication

Ask what the patient already understands, what worries them most and what outcome matters to them.
Use open questions first, then focused questions; do not interrupt unnecessarily.
Recognise the patient as a partner, not merely a diagnosis or bed number.
Offer choices when clinically safe and explain when an emergency limits choice.
Include family or carers with permission, while preserving the competent patient’s privacy.
Use trauma-informed principles: safety, trust, choice, collaboration and empowerment.
For children, communicate at their developmental level and obtain appropriate caregiver consent and child assent.

Language, culture, disability and health literacy

Communication must be adapted, not merely translated. Language barriers can reduce patient satisfaction and the quality of care, while health-literacy barriers arise when information is too difficult to find, understand or use.

Use a trained interpreter when available; avoid using children as interpreters for complex, sensitive or consent discussions.
Speak to the patient, not only the interpreter; use short sentences and pause for interpretation.
Ask about preferred language, hearing/vision needs, reading ability and communication devices.
Respect cultural beliefs while explaining what is medically urgent and what cannot safely be delayed.
Use pictures, demonstrations, translated materials and teach-back.
Do not assume that nodding, silence or smiling means understanding or agreement.

Teach-back example: “I want to make sure I explained it clearly. Can you tell me in your own words what you will do if the breathing becomes worse?” This checks the explanation, not the patient’s intelligence.

Barriers to communication

Barrier	Examples	Practical response
Physical/environmental	Noise, crowding, poor lighting, distance, pain and lack of privacy.	Move closer, reduce noise, provide privacy and choose a safe position.
Physiological	Breathlessness, deafness, delirium, aphasia, fatigue or reduced consciousness.	Stabilise first, use aids, simplify and involve the appropriate specialist/carer.
Semantic/language	Jargon, dialect differences, unfamiliar abbreviations and poor translation.	Use plain language, interpreter support and teach-back.
Psychological	Fear, grief, anger, shame, denial, stigma or previous trauma.	Acknowledge emotion, allow time and avoid confrontation.
Cultural/social	Different beliefs, gender norms, power distance, literacy or family roles.	Ask respectfully, avoid assumptions and negotiate safe care.
Organisational	Staff shortage, hierarchy, interruptions, unclear responsibility and poor handover.	Use structured tools, clarify roles and protect handover time.
Technological	Network failure, wrong recipient, incompatible system or downtime.	Verify identity, use approved backup channels and document later reconciliation.

Confidentiality, privacy and professional boundaries

Share information only with people who need it for care, safeguarding, referral, teaching or lawful reporting.
Confirm the recipient before telephone, radio, email or electronic-record disclosure.
Do not discuss identifiable patients in public areas, social media, personal messaging groups or unauthorised devices.
Obtain permission before photographs, recordings, observers or student teaching, and follow facility policy.
Explain limits of confidentiality where there is serious risk, abuse, public-health duty or legal requirement.
Maintain boundaries: do not promise secrecy, accept inappropriate gifts, form exploitative relationships or give personal medical advice outside your role.

Consent and shared decisions

Consent is a communication process, not merely a signature. The person needs relevant information about the proposed assessment or intervention, benefits, material risks, alternatives and the option to refuse. Assess capacity for the specific decision, communicate in an accessible way and document the discussion.

Explain who you are and what you propose to do.
Explain why it is needed, what it may feel like and what alternatives exist.
Invite questions and check understanding.
Confirm voluntary agreement without coercion.
Document consent, refusal, capacity concerns, interpreter use and urgent best-interest decisions.

Team communication and closed-loop safety

Closed-loop communication means the sender gives a clear instruction, the receiver repeats it, and the sender confirms completion. It is especially important during resuscitation, medication administration, transfer and procedures.

Address a named person: “Amina, please attach the ECG leads.”
Receiver repeats: “Attaching ECG leads now.”
Receiver reports completion and findings: “ECG attached; rhythm is narrow-complex tachycardia.”
Leader acknowledges, interprets and gives the next action.

SBAR — Situation: what is happening now; Background: relevant history; Assessment: findings and concern; Recommendation/request: what you need and by when.

Communication during handover

Identify the patient with at least two approved identifiers and state the urgency.
Give the presenting problem, relevant history, allergies, medications, vital trends, examination, interventions, response and outstanding risks.
Use time-critical language: “I am concerned about impending airway compromise; senior airway review is needed now.”
Invite questions, ask the receiving person to repeat critical information and document the handover.
Perform bedside handover when safe, involving the patient and respecting privacy.

Communication in difficult situations

Anger: remain calm, acknowledge the concern, set respectful limits and move to a safer space if needed.
Bad news: use a quiet setting, assess what the person knows, give information in small portions, allow silence and offer support.
Refusal: explore the reason, assess capacity, explain risks and alternatives, respect an informed refusal and document.
Confusion or delirium: use short orientation statements, reduce stimulation, involve carers and assess urgent causes.
Grief: avoid forced reassurance; listen, acknowledge loss and connect the person to support.
Safeguarding: listen privately, avoid leading questions, record the person’s words and follow the reporting pathway.

Written communication foundations

Written communication must be factual, legible, dated, timed, attributable and sufficiently detailed for another professional to act safely. Record observations rather than insults or unsupported conclusions. Correct errors according to policy; never erase, backdate or falsify a record.

Use approved abbreviations only and write units for numbers, doses and measurements.
Separate patient statements, objective findings, clinical interpretation and plan.
Document advice, consent, refusal, escalation, response and follow-up.
Use neutral language: “patient shouted and pushed the trolley” rather than “patient is difficult.”
Protect electronic records with individual logins, screen privacy and secure passwords.

Communication quality checklist

Before	During	After
Clarify purpose, audience, urgency and privacy.	Use plain language, active listening, empathy and appropriate pace.	Confirm understanding, document and arrange follow-up.
Check identity, interpreter and communication aids.	Observe verbal and non-verbal cues; invite questions.	Share only necessary information through approved channels.
Gather accurate facts and anticipate barriers.	Use closed-loop communication for safety-critical tasks.	Reflect on what worked and what needs improvement.

Scenario-based application

Scenario 1 — language barrier: A patient with chest pain speaks little English and a relative offers to translate. Stabilise and assess immediately, obtain a trained interpreter as soon as possible, use short sentences, explain consent and use teach-back. Do not let translation delay life-saving treatment, but do not use a child for a complex consent discussion.

Scenario 2 — unsafe handover: During transfer, the receiving team is told only “the patient is stable.” The EMT instead uses SBAR: current airway/breathing status, blood pressure trend, allergy, treatment, response and specific concern. The receiving clinician repeats the critical risks and confirms the plan.

Scenario 3 — angry relative: A relative shouts that staff are ignoring the patient. The nurse moves to a safer private area, acknowledges the fear, explains what is being done, gives a realistic time frame, sets respectful boundaries and escalates security only if safety is threatened.

Scenario 4 — teach-back: Before discharge after an asthma emergency, the EMT asks the patient to explain when to use the reliever, which warning signs require urgent help and where to return. The patient’s answer reveals misunderstanding, so the explanation is corrected before leaving.

Common errors to avoid

Using jargon, unexplained abbreviations or vague phrases such as “the patient is okay.”
Interrupting, dismissing emotion, arguing or giving false reassurance.
Assuming silence, nodding or a signature proves understanding.
Sharing patient information in public, on personal social media or with an unverified recipient.
Failing to identify a named person for an urgent task.
Not documenting refusal, advice, escalation or the patient’s response.
Allowing hierarchy or fear to silence a safety concern.

Personal communication improvement plan

Choose one observable goal, such as “I will use teach-back for every high-risk discharge.”
Practise with role-play: emergency handover, angry relative, informed refusal and language barrier.
Ask a colleague or educator for specific feedback on clarity, listening, tone and completeness.
Review one written note or handover each week for missing safety information.
Repeat the cycle and measure improvement using patient questions, error reports, feedback and confidence.

Quick revision questions

Define communication and list the elements of the communication process.
Differentiate verbal, non-verbal, written, visual and electronic communication.
Explain the 7 Cs and give a clinical example of each.
List six communication barriers and one solution for each.
What is the purpose of feedback, teach-back and closed-loop communication?
What information belongs in an SBAR handover?
How can a health worker protect confidentiality during electronic communication?
Why is consent a process rather than a signature?

Key takeaways

Communication is complete only when the receiver understands and can act safely.
Adapt every message to urgency, culture, language, disability, emotion and health literacy.
Use empathy with patients and assertiveness with teams; both protect safety.
SBAR, read-back and closed-loop communication reduce omissions during emergencies.
Protect privacy, document accurately and treat communication as a clinical intervention.

Hyponatraemia and Hypernatraemia: Emergency Assessment, Neurological Risks and Safe Correction

Why this matters to emergency medicine students: Sodium disorders change brain-cell water content. Acute hyponatraemia can cause cerebral oedema, seizures, herniation and respiratory arrest; hypernatraemia can cause cellular dehydration, intracranial bleeding, seizures and coma. Correction that is too slow may leave the patient in danger, while correction that is too fast can cause osmotic demyelination or cerebral oedema. Emergency care therefore combines ABCDE resuscitation, neurological assessment, confirmation of the result, volume-status reasoning, carefully selected fluid and frequent sodium checks. Use the current Uganda/local electrolyte protocol and senior guidance for exact bolus volumes and correction limits.

Learning objectives

Define hypo- and hypernatraemia and explain their effects on the brain.
Classify causes by volume status and identify dangerous acute symptoms.
Perform ABCDE assessment, confirm sodium abnormalities and investigate the cause.
Treat severe symptomatic hyponatraemia with monitored hypertonic saline and avoid overcorrection.
Restore perfusion in hypernatraemic shock, calculate free-water needs and replace water safely.
Plan nursing monitoring, prevention, education and follow-up.

Sodium physiology and definitions

Sodium is the major extracellular cation and a principal determinant of extracellular osmolality. Water moves across cell membranes toward the higher effective osmolality; rapid changes therefore cause brain swelling or shrinkage. Hyponatraemia is usually serum sodium below 135 mmol/L and hypernatraemia above 145 mmol/L, but symptoms depend on speed of change, tonicity, age, comorbidities and the cause.

Hyponatraemia: causes by volume status

Type	Common causes	Examination clues
Hypovolaemic	Vomiting, diarrhoea, bleeding, burns, sweating, diuretics, adrenal insufficiency or renal salt wasting.	Postural dizziness, dry mucosae, tachycardia, low JVP, poor skin turgor and oliguria.
Euvolaemic	SIADH, CNS disease, pulmonary disease, medicines, adrenal insufficiency, hypothyroidism or excess water intake.	No clear oedema or dehydration; urine may be inappropriately concentrated.
Hypervolaemic	Heart failure, cirrhosis, nephrotic syndrome or advanced kidney failure.	Oedema, ascites, raised JVP, crackles and weight gain.
Non-hypotonic	Hyperglycaemia, mannitol or laboratory artefact/pseudohyponatraemia.	Clinical picture may not match a true hypotonic state.

Hypernatraemia: causes by water balance

Water loss greater than sodium loss: fever, sweating, diarrhoea, vomiting, burns, osmotic diuresis or inadequate access to water.
Renal water loss: central or nephrogenic diabetes insipidus, diuretics and kidney concentrating failure.
Excess sodium: concentrated sodium bicarbonate, salt ingestion, hypertonic infusions or mineralocorticoid states.
Vulnerable groups: infants, older adults, confused or immobile patients, people dependent on carers and patients with impaired thirst.

Clinical features and red flags

Hyponatraemia

Nausea, vomiting, headache, lethargy, muscle cramps, weakness and unsteadiness.
Confusion, agitation, reduced consciousness, seizures, coma, respiratory arrest and signs of cerebral oedema.
Acute symptoms can be severe even when the sodium value is not extremely low; chronic adaptation may mask symptoms.

Hypernatraemia

Intense thirst, dry mucosae, irritability, weakness, twitching and restlessness.
Confusion, hyperreflexia, seizures, coma, intracranial bleeding and shock.
Infants may have poor feeding, high-pitched cry, fewer wet nappies and irritability; older adults may present with delirium or falls.

Immediate escalation: seizure, coma, severe confusion, respiratory compromise, shock, rapidly changing sodium, sodium below about 120 mmol/L with symptoms, sodium above about 160 mmol/L, or suspected diabetes insipidus, adrenal crisis, poisoning or CNS disease.

First contact and safety

Call for help, place the patient in a monitored area and bring seizure/airway equipment.
Check ABCDE, bedside glucose, temperature, vital signs, fluid balance and neurological status.
Protect the airway during seizures or vomiting; position safely and do not force oral fluids in a drowsy patient.
Obtain IV access and a properly collected blood sample; repeat a surprising result without delaying treatment of severe neurological symptoms.
Review recent fluids, medicines, renal/endocrine history, water intake, losses and the timeline of symptoms.

ABCDE assessment

A — Airway

Assess protective reflexes, secretions and aspiration risk, particularly during seizures or reduced consciousness.
Prepare suction and airway support; consider early anaesthesia/critical-care help if cerebral oedema or repeated seizures are present.

B — Breathing

Assess respiratory rate, oxygen saturation, effort and postictal ventilation.
Give oxygen for hypoxaemia and support ventilation if neurological deterioration causes apnoea.

C — Circulation

Assess pulse, blood pressure, capillary refill, JVP, oedema, mucous membranes, weight and urine output.
In shock, restore perfusion first with an appropriate isotonic crystalloid even if sodium is high; then correct the water deficit under close monitoring.

D — Disability

Record GCS/AVPU, pupils, seizure activity, focal deficits, headache, nausea and glucose.
Treat seizures according to the local seizure protocol while urgently correcting the sodium-related cause.

E — Exposure

Look for diarrhoea, vomiting, burns, infection, oedema, ascites, medications, IV fluids and signs of diabetes insipidus.
Measure temperature and prevent heat loss or ongoing environmental water loss.

Investigations

Repeat serum sodium, potassium, chloride, bicarbonate, urea, creatinine, glucose, calcium and magnesium.
Measure serum osmolality to distinguish hypotonic, isotonic and hypertonic states; correct the sodium interpretation for marked hyperglycaemia under local guidance.
Urine osmolality and urine sodium help distinguish SIADH, hypovolaemia, renal salt loss and diabetes insipidus.
Blood gas, lactate and ketones for shock, DKA or severe illness.
Thyroid and cortisol testing when endocrine disease is possible; do not delay emergency steroid treatment in suspected adrenal crisis.
ECG and imaging guided by seizures, trauma, CNS disease, heart failure or pulmonary symptoms.

Severe symptomatic hyponatraemia

Seizures, coma, severe confusion, respiratory compromise or signs of cerebral oedema are emergencies. Treatment aims to raise sodium promptly enough to reduce cerebral swelling, not to normalise it immediately.

Move to resuscitation/critical-care monitoring, protect the airway and treat seizures.
Give a protocol-directed bolus of 3% hypertonic saline, commonly 100–150 mL over 10–20 minutes in adults, then reassess symptoms and sodium. It may be repeated under senior guidance until symptoms improve or a small initial rise (often 4–6 mmol/L) is achieved.
Check sodium frequently, watch urine output and stop hypertonic saline once the emergency neurological symptoms improve or the safe initial rise is reached.
Do not exceed the local maximum correction limit—often no more than 8 mmol/L in 24 hours for high-risk patients and approximately 8–10 mmol/L in 24 hours overall, with a conservative 48-hour limit.
If overcorrection occurs, call endocrinology/critical care urgently; controlled free-water replacement and desmopressin may be used by specialists.

Important: Hypertonic saline is a monitored emergency therapy. Never improvise the concentration or infusion rate. Treat the cause after the immediate cerebral threat is controlled.

Cause-specific hyponatraemia treatment

Hypovolaemic: restore extracellular volume with isotonic crystalloid, stop losses and monitor for a sudden water diuresis and rapid sodium rise.
SIADH/euvolemic: stop offending medicines, restrict free water under medical supervision, treat the cause and seek specialist advice for persistent or severe cases.
Heart failure/cirrhosis/nephrotic syndrome: manage congestion, fluid and salt balance with the medical team; avoid reflexive large saline volumes.
Adrenal insufficiency: treat suspected adrenal crisis urgently with steroid and fluid protocols.
Hyperglycaemia or mannitol: treat the osmotic cause and interpret sodium in relation to tonicity.

Hypernatraemia management

Restore circulation: if shocked or severely hypovolaemic, give isotonic crystalloid first until perfusion improves.
Replace free water: allow oral/enteral water if alert and safe to swallow; use IV 5% dextrose or another appropriate hypotonic solution when oral intake is impossible.
Calculate and plan: estimate free-water deficit with the clinical team, include ongoing losses and reassess frequently.
Correct safely: chronic or unknown-duration hypernatraemia is commonly lowered no faster than about 0.5 mmol/L/hour or 10–12 mmol/L/day to reduce cerebral oedema risk.
Find the cause: treat fever, diarrhoea, hyperglycaemia, diabetes insipidus, medication effects, obstruction or excessive sodium administration.
Monitor: sodium, neurological state, urine output, glucose, fluid balance and signs of pulmonary oedema.

Acute sodium loading or acute hypernatraemia may require a different rate under specialist supervision. Do not apply a fixed rate without knowing the duration, volume status and ongoing losses.

Neurological complications of correction

Risk	Mechanism	Prevention/response
Cerebral oedema	Serum sodium falls rapidly or hypernatraemia is corrected too quickly.	Frequent sodium checks, controlled free water and urgent neurological review.
Osmotic demyelination	Chronic hyponatraemia is corrected too rapidly, especially with alcoholism, malnutrition, liver disease or hypokalaemia.	Conservative correction limits; specialist relowering if overcorrection occurs.
Seizure or coma	Acute brain water shift, severe sodium abnormality or underlying CNS disease.	Airway protection, seizure protocol and cause-specific sodium treatment.
Rebound abnormality	Ongoing diarrhoea, diuresis, diabetes insipidus or inappropriate fluid continuation.	Strict balance chart, repeat labs and adjust fluids promptly.

Nursing interventions

Perform and document frequent neurological observations, seizure precautions and airway checks.
Use an infusion pump for hypertonic or hypotonic therapy and independently verify the fluid and rate.
Record every oral, IV, enteral and urinary volume; measure urine output accurately.
Repeat serum sodium at the prescribed interval and report a faster-than-planned correction immediately.
Monitor respiratory status, oedema, lung sounds, JVP, blood pressure and glucose.
Explain why patients must not self-correct severe sodium abnormalities by drinking large volumes or taking salt tablets.
Maintain dignity and safety for confused patients; prevent falls and aspiration.

Admission, escalation and monitoring

Admit symptomatic, severe, rapidly changing or uncertain sodium disorders; use high-dependency/ICU care for seizures, coma, shock or airway compromise.
Involve nephrology/endocrinology for severe, refractory, endocrine, renal or overcorrection cases.
Repeat sodium frequently during hypertonic saline, active free-water replacement, brisk diuresis or unstable illness.
Do not discharge until symptoms are stable, the cause and fluid plan are understood and reliable follow-up is arranged.

Scenario-based application

Scenario 1 — symptomatic hyponatraemia: A patient taking a thiazide has headache, vomiting, confusion and a seizure with sodium 116 mmol/L. Protect the airway, place on monitoring, treat the seizure, give protocol-directed 3% saline bolus under senior supervision, check sodium frequently and stop the thiazide. Do not wait for a complete endocrine work-up before treating cerebral symptoms.

Scenario 2 — hypernatraemic shock: An older patient with diarrhoea is confused, tachycardic, hypotensive and sodium 168 mmol/L. Restore perfusion first with isotonic crystalloid, then calculate and replace free water gradually, treating ongoing losses and monitoring sodium/urine output. Rapidly giving large volumes of hypotonic fluid before circulation is restored can be dangerous.

Scenario 3 — overcorrection risk: A hypovolaemic hyponatraemic patient begins passing large volumes of dilute urine after saline. Check sodium frequently, stop or adjust the correcting fluid, call senior/endocrine support and consider controlled relowering therapy if the safe limit is being exceeded.

Prevention and education

Review diuretics, antidepressants, antiepileptics, desmopressin, steroids and other medicines after illness or dose changes.
Ensure older, confused, dependent or febrile patients have regular access to safe water and monitoring.
Manage vomiting, diarrhoea, fever, burns, diabetes and kidney disease early.
Teach high-risk patients not to overdrink water, take salt tablets or use sports drinks as a substitute for clinical review.
Arrange repeat electrolytes after discharge and provide clear seizure, confusion, weakness and dehydration return precautions.

Common errors to avoid

Treating the sodium number without assessing tonicity, volume status, glucose and symptoms.
Giving large amounts of isotonic saline to a congested patient or hypotonic fluid to an underevaluated shock patient.
Correcting chronic hyponatraemia too rapidly and causing osmotic demyelination.
Lowering chronic hypernatraemia too rapidly and provoking cerebral oedema.
Failing to recheck sodium after a fluid change or during sudden diuresis.
Allowing a confused or seizing patient to drink unsupervised.
Missing adrenal crisis, SIADH, diabetes insipidus, hyperglycaemia or kidney failure.

Documentation checklist

Onset, symptoms, suspected duration, fluid intake/losses, medicines and comorbidities.
ABCDE and neurological findings, seizures, glucose, volume-status assessment and urine output.
Serum/urine osmolality, urine sodium, electrolytes, renal/endocrine tests and serial sodium results.
Fluid type, volume, rate, start/stop times, correction target and response.
Senior/endocrine/nephrology decisions, escalation, education and follow-up.

Quick revision questions

How does acute hyponatraemia cause seizures and coma?
Classify hyponatraemia into hypovolaemic, euvolaemic and hypervolaemic causes.
What are the first priorities for a patient with a hyponatraemic seizure?
Why should sodium correction be limited in chronic hyponatraemia?
What should be done first in a shocked patient with hypernatraemia?
What is the purpose of free-water replacement and how is it monitored?
Which medicines and endocrine disorders commonly cause sodium abnormalities?
What nursing observations detect overcorrection early?

Key takeaways

Neurological symptoms and the speed of sodium change determine urgency—not the number alone.
Severe symptomatic hyponatraemia needs monitored hypertonic saline; do not delay for tests.
Hypernatraemic shock needs perfusion restoration first, followed by carefully controlled free-water replacement.
Frequent sodium, glucose, fluid-balance and neurological checks prevent treatment-related harm.
Always identify and correct the underlying renal, endocrine, medication, gastrointestinal or access-to-water problem.

Hypokalaemia and Hyperkalaemia: Emergency Assessment, ECG Recognition and Treatment

Why this matters to emergency medicine students: Potassium controls resting membrane potential, neuromuscular function and cardiac conduction. A dangerously low or high serum potassium can cause weakness, respiratory failure, ventricular dysrhythmia or cardiac arrest, sometimes with few symptoms. The emergency priorities are to confirm the result without delaying care, obtain an ECG, identify the cause, protect the myocardium when necessary, shift or remove potassium safely, replace deficits carefully and monitor for rebound or treatment complications. Always use the current Uganda/local electrolyte protocol for exact concentrations, infusion rates and monitoring requirements.

Learning objectives

Explain potassium physiology and the difference between a concentration problem and a total-body deficit or excess.
Recognise symptoms and ECG changes of hypokalaemia and hyperkalaemia.
Identify renal, gastrointestinal, endocrine, medication, acid–base and cellular-shift causes.
Manage life-threatening hyperkalaemia and severe hypokalaemia using a structured ABCDE approach.
Replace potassium safely, correct magnesium, monitor glucose/ECG/urine output and prevent recurrence.

Potassium physiology

Most potassium is intracellular. The sodium–potassium pump, insulin, catecholamines and acid–base balance move potassium between the intracellular and extracellular spaces, while the kidneys determine long-term excretion. A normal serum value can occasionally hide a depleted total-body store, and a high value can be caused by a shift out of cells rather than excess total potassium. Treat the patient and the cause, not the number alone.

Definitions and severity

Disorder	Common definition	Clinical emergency concern
Hypokalaemia	Serum K+ below about 3.5 mmol/L.	Risk increases with K+ ≤3.0, rapid fall, ECG change, weakness, digoxin use or heart disease.
Severe hypokalaemia	Often K+ below 2.5 mmol/L or symptomatic/ECG-positive.	Potential paralysis, respiratory failure and ventricular arrhythmia; urgent monitored replacement.
Hyperkalaemia	Serum K+ above the laboratory upper limit, often ≥5.5 mmol/L.	Risk is urgent with ECG change, symptoms, rapid rise or K+ around ≥6.0–6.5 mmol/L depending on protocol.
Life-threatening dyskalaemia	Any potassium value with malignant rhythm, severe weakness, shock or cardiac conduction disturbance.	Resuscitation and treatment should begin while confirmation is obtained.

Causes of hypokalaemia

Reduced intake: malnutrition, prolonged fasting, alcoholism or inability to swallow.
Gastrointestinal loss: vomiting, diarrhoea, fistula, laxative misuse or high-output stoma.
Renal loss: loop/thiazide diuretics, osmotic diuresis, renal tubular disease, mineralocorticoid excess or certain antibiotics.
Cellular shift: insulin, beta-agonists, alkalosis, refeeding and periodic paralysis.
Low magnesium: promotes renal potassium wasting and makes replacement difficult.
Endocrine: hyperaldosteronism, Cushing syndrome and some inherited tubulopathies.

Causes of hyperkalaemia

Reduced excretion: acute kidney injury, chronic kidney disease, adrenal insufficiency, hypoaldosteronism or urinary obstruction.
Medicines: potassium supplements, ACE inhibitors, ARBs, mineralocorticoid antagonists, potassium-sparing diuretics, NSAIDs, trimethoprim, heparin and some chemotherapy.
Cellular release: metabolic acidosis, insulin deficiency, rhabdomyolysis, tumour lysis, haemolysis, burns and massive tissue injury.
Excess intake: usually important when kidney excretion is impaired or a medication blocks excretion.
Pseudohyperkalaemia: haemolysis, prolonged tourniquet/fist clenching, delayed processing, thrombocytosis or leukocytosis.

Clinical features

Hypokalaemia

Fatigue, cramps, myalgia, paraesthesia, constipation or ileus.
Generalised weakness, hyporeflexia, ascending paralysis and respiratory muscle weakness in severe cases.
Palpitations, syncope and dysrhythmia; symptoms may be absent despite a dangerous ECG.
Polyuria and polydipsia when renal concentrating ability is impaired.

Hyperkalaemia

Often asymptomatic until the rhythm becomes unstable.
Perioral or limb paraesthesia, muscle weakness, flaccid paralysis, nausea or abdominal discomfort.
Palpitations, chest discomfort, syncope, bradycardia or sudden collapse.

Immediate contact and safety

Use ABCDE and call for help if the patient is weak, confused, hypotensive, breathless or has an abnormal rhythm.
Place the patient on continuous cardiac monitoring and obtain a 12-lead ECG urgently.
Confirm the potassium result with a non-haemolysed sample when pseudohyperkalaemia is plausible, but do not delay treatment for ECG-positive or unstable hyperkalaemia.
Establish IV access, check bedside glucose and review medicines, kidney function, urine output and recent fluid losses.
Stop potassium-containing fluids and medications that worsen the abnormality while a senior clinician reviews the full prescription.

ABCDE assessment

A and B — Airway and breathing

Assess speech, respiratory effort and ability to protect the airway.
Weakness or paralysis may impair ventilation; provide oxygen for hypoxaemia and prepare assisted ventilation if required.

C — Circulation

Check pulse, blood pressure, capillary refill, peripheral temperature and rhythm.
Treat dysrhythmia as a resuscitation emergency and prepare defibrillation/pacing equipment.
Assess volume status, urine output and evidence of kidney failure, sepsis, burns or rhabdomyolysis.

D and E — Disability and exposure

Check GCS, glucose, muscle power, reflexes, sensation, cramps, bowel sounds and pain.
Look for burns, crush injury, renal disease, dehydration, diarrhoea, vomiting or medication patches and infusions.

ECG patterns

Hypokalaemia	Hyperkalaemia
Flattened or inverted T waves, ST depression and prominent U waves.	Early peaked T waves and shortened QT.
Prolonged QU interval, atrial or ventricular ectopy.	PR prolongation, flattened/absent P waves and QRS widening.
Torsades, ventricular tachycardia, fibrillation or arrest in severe cases.	Sine-wave pattern, ventricular fibrillation, pulseless electrical activity or asystole.
ECG can be normal despite severe depletion.	A normal ECG does not exclude sudden deterioration; continue monitoring.

PEAK-K for dangerous hyperkalaemia: Peaked T waves, Extended PR, Absent P waves, Killer QRS/sine wave. For hypokalaemia think U waves and prolonged QU.

Investigations

Repeat electrolytes using a properly collected sample; check sodium, chloride, bicarbonate, magnesium, calcium, phosphate, urea and creatinine.
Venous or arterial blood gas for pH, bicarbonate, lactate and urgent potassium when laboratory delay is significant.
Glucose to identify insulin deficiency, diabetic ketoacidosis or treatment-related hypoglycaemia.
Urine potassium and acid–base testing when renal wasting or endocrine causes are suspected.
Creatine kinase, urinalysis and renal assessment for rhabdomyolysis or tumour lysis.
Digoxin level when toxicity is possible; review all medicines, supplements and salt substitutes.
Serial ECGs and repeat potassium after every urgent intervention.

Emergency management of hyperkalaemia

Management has three simultaneous goals: protect the cardiac membrane, shift potassium into cells and remove potassium from the body. A normal ECG does not guarantee safety.

1. Stabilise the myocardium

For ECG changes, malignant arrhythmia or severe hyperkalaemia with clinical instability, give IV calcium under the local protocol. Calcium antagonises membrane excitability but does not lower serum potassium.
Reassess the ECG after administration and repeat calcium if changes persist according to senior/local guidance.
Use a secure IV line and monitor for extravasation; calcium chloride is more concentrated and more tissue-irritant than calcium gluconate.

2. Shift potassium intracellularly

Give IV insulin with glucose according to protocol; check glucose before treatment and monitor repeatedly for delayed hypoglycaemia, especially in kidney failure.
Nebulised salbutamol can provide additional intracellular shift, but response may be variable and it does not replace insulin/glucose or calcium when indicated.
Consider bicarbonate only for selected patients with significant metabolic acidosis and senior advice; it is not routine monotherapy.

3. Remove potassium from the body

Stop exogenous potassium and offending medicines; treat the underlying cause.
Use a loop diuretic only if the patient can produce urine and volume status allows.
Use an appropriate potassium binder when available and suitable, understanding that onset is slower than membrane stabilisation and cellular shifting.
Arrange urgent dialysis for refractory or severe hyperkalaemia, anuria, advanced kidney failure, severe acidosis, ongoing tissue breakdown or recurrent arrhythmia.

Emergency management of hypokalaemia

Place the patient on ECG monitoring when severe, symptomatic, rapidly falling, digoxin-treated or associated with ECG changes.
Identify and stop ongoing losses where possible: review diuretics, laxatives, vomiting, diarrhoea and renal wasting.
Measure and correct magnesium because low magnesium promotes continued potassium loss and refractory replacement.
Use oral potassium for stable, mild-to-moderate hypokalaemia when the gut works and there is no urgent ECG or neuromuscular threat.
Use IV potassium for severe/symptomatic hypokalaemia, ECG changes, paralysis or inability to absorb orally. Use a pump, a secure line, the prescribed concentration and the local maximum rate—never give IV potassium as a rapid push.
Recheck potassium, magnesium, renal function and ECG after replacement; avoid overshoot, especially in kidney disease.

Medication and cause-specific management

Diuretics: review indication and dose; replace losses and consider a potassium-sparing strategy only under clinician supervision.
DKA or insulin therapy: follow the DKA protocol; insulin can lower potassium rapidly, so assess potassium before and during treatment.
Renal failure: adjust replacement and medication, involve nephrology early and consider dialysis for severe hyperkalaemia.
Gastrointestinal loss: restore volume, potassium and magnesium and treat vomiting/diarrhoea.
Rhabdomyolysis or tumour lysis: manage the cause, renal injury and rapidly rising potassium in a critical-care setting.
Adrenal insufficiency: assess shock, glucose and sodium; give urgent steroid therapy under the relevant emergency protocol.

Monitoring after treatment

Monitor	Why it matters	Escalate when
Continuous ECG	Detects recurrent or treatment-related dysrhythmia.	New QRS widening, bradycardia, ventricular ectopy, VT or arrest.
Potassium	Confirms response and detects rebound or overcorrection.	Persistent severe value, rapid change or mismatch with clinical state.
Glucose after insulin	Insulin–glucose treatment can cause delayed hypoglycaemia.	Falling glucose, altered mental state or recurrent low readings.
Renal function and urine	Determines excretion and replacement safety.	Oliguria, rising creatinine, anuria or fluid overload.
Neuromuscular status	Tracks weakness, paralysis and recovery.	Respiratory weakness, inability to walk or progressive paralysis.

Nursing interventions

Confirm the sample, label the urgency and report critical values immediately.
Maintain continuous ECG monitoring and document rhythm changes with times and interventions.
Use an infusion pump and independent double-check for IV potassium, calcium, insulin and concentrated electrolytes.
Check IV patency, inspect for extravasation and never administer IV potassium by bolus.
Monitor capillary glucose frequently after insulin–glucose therapy and provide rescue glucose according to protocol.
Measure urine output, fluid balance, neurological status, muscle power and respiratory effort.
Educate about medication, salt substitutes, supplements, renal follow-up and dietary advice from the clinical team.

Complications

Ventricular tachycardia, ventricular fibrillation, conduction block and sudden cardiac arrest.
Respiratory failure from muscle weakness or fluid overload.
Rhabdomyolysis, acute kidney injury and metabolic acidosis.
Hypoglycaemia after insulin therapy, tissue injury from extravasated calcium and potassium, and rebound hyperkalaemia.
Neurological injury from hypoperfusion, falls and prolonged paralysis.

Scenario-based application

Scenario 1 — hyperkalaemia with ECG changes: A patient with renal failure has weakness, K+ 7.1 mmol/L and broad QRS complexes. Start continuous ECG, call for help, give IV calcium under protocol, shift potassium with insulin–glucose and salbutamol, stop offending medicines, monitor glucose and arrange urgent dialysis review. Do not wait for a repeat result before treating the ECG-positive emergency.

Scenario 2 — severe hypokalaemia: A patient with prolonged diarrhoea has K+ 2.1 mmol/L, U waves and leg weakness. Admit to a monitored area, check magnesium and renal function, begin controlled IV potassium replacement using a pump and local maximum rate, treat diarrhoeal losses and repeat ECG/electrolytes.

Scenario 3 — pseudohyperkalaemia: An asymptomatic patient has a haemolysed sample showing K+ 6.4 mmol/L, a normal ECG and normal renal function. Repeat an urgently collected non-haemolysed sample while maintaining monitoring and reviewing the result; if ECG or symptoms develop, treat as true hyperkalaemia.

Prevention and patient education

Review renal function and electrolytes after medication changes, illness, vomiting, diarrhoea or diuretic adjustment.
Do not self-start potassium tablets, herbal remedies or potassium-containing salt substitutes.
Teach people with kidney disease or heart failure which medicines and foods require professional advice.
Provide sick-day guidance where appropriate and ensure access to follow-up blood testing.
Prevent recurrent diarrhoea, vomiting, malnutrition and uncontrolled diabetes.

Common errors to avoid

Treating the laboratory number without an ECG, repeat sample or cause assessment.
Assuming a normal ECG rules out dangerous hyperkalaemia.
Giving calcium as if it removes potassium—it stabilises the myocardium only.
Giving insulin without glucose planning and prolonged glucose monitoring.
Giving IV potassium by bolus, using an unmonitored infusion or ignoring renal failure.
Failing to correct magnesium in refractory hypokalaemia.
Discharging a symptomatic, severe or ECG-positive patient without monitored follow-up.

Documentation checklist

Symptoms, onset, comorbidities, medicines, supplements, fluid losses and kidney function.
Initial and repeat potassium, magnesium, glucose, acid–base results and ECG findings.
Time, dose, route and response to calcium, insulin/glucose, beta-agonist, potassium and fluids.
Monitoring frequency, urine output, adverse events, senior/nephrology discussion and disposition.
Cause-specific prevention advice, medication changes and follow-up plan.

Quick revision questions

Why can a serum potassium value misrepresent total-body stores?
List five causes of hypokalaemia and five causes of hyperkalaemia.
What ECG changes suggest dangerous hyperkalaemia?
What are the three simultaneous treatment goals in severe hyperkalaemia?
Why must magnesium be checked in hypokalaemia?
When is IV rather than oral potassium replacement appropriate?
Why is glucose monitoring essential after insulin–glucose therapy?
When should urgent dialysis be considered?

Key takeaways

Dyskalaemia can kill through electrical instability before obvious symptoms appear.
ECG monitoring and a structured ABCDE assessment are essential in severe or symptomatic cases.
Hyperkalaemia treatment protects the heart, shifts potassium into cells and removes potassium from the body.
Hypokalaemia requires controlled replacement, magnesium correction and repeated ECG/electrolyte checks.
Always treat the cause and plan follow-up; prevention is safer than repeated emergency replacement.

Hypersensitivity Reactions and Anaphylaxis: Recognition, Resuscitation and Emergency Management

Why this matters to emergency medicine students: Hypersensitivity ranges from a local itchy rash to rapidly fatal airway obstruction and distributive shock. Anaphylaxis is a clinical emergency in which airway, breathing or circulation may deteriorate within minutes, sometimes without a rash. Early intramuscular adrenaline, correct positioning, oxygen, fluid resuscitation and repeated reassessment save lives. This lesson covers immune mechanisms, urticaria and angio-oedema, anaphylaxis, drug reactions, observation, discharge and prevention. Use the current Uganda/local anaphylaxis protocol for exact preparation, age-based dose and escalation.

Learning objectives

Classify hypersensitivity reactions and distinguish common allergic symptoms from anaphylaxis.
Recognise airway, breathing and circulation threats, including anaphylaxis without skin signs.
Give immediate first aid and intramuscular adrenaline safely, with appropriate positioning and repeat dosing.
Manage bronchospasm, shock, angio-oedema, refractory reactions and cardiac arrest with senior support.
Plan monitoring, observation, discharge education, trigger avoidance, referral and documentation.

What is hypersensitivity?

Hypersensitivity is an exaggerated or inappropriate immune response to an antigen. It may be allergic (often IgE-mediated) or non-IgE-mediated, such as direct mast-cell activation by some medicines, radiocontrast or physical triggers. The emergency practitioner treats the physiology rather than waiting to prove the mechanism.

Classification of hypersensitivity

Type	Main mechanism	Examples relevant to emergency care
Type I: immediate	IgE-mediated mast-cell and basophil mediator release.	Anaphylaxis, urticaria, angio-oedema, allergic asthma, food or venom reactions.
Type II: antibody-mediated	IgG/IgM targets cell or tissue antigens.	Drug-induced haemolysis, thrombocytopenia and some transfusion reactions.
Type III: immune complex	Deposited antigen–antibody complexes cause inflammation.	Serum sickness-like reactions and some vasculitic drug reactions.
Type IV: delayed T-cell mediated	Cell-mediated inflammation, usually hours to days later.	Contact dermatitis, delayed drug eruptions and SJS/TEN spectrum reactions.

Common triggers and risk factors

Foods such as nuts, seeds, eggs, milk, fish, shellfish and hidden ingredients.
Medicines, especially antibiotics, analgesics, anaesthetic agents, vaccines and biologic products.
Bee, wasp and other insect venom; latex; blood products; antiseptics and occupational exposures.
Exercise, cold, heat, pressure, alcohol or co-factors that amplify a food or drug reaction.
Asthma, mast-cell disorders, cardiovascular disease, beta-blocker/ACE-inhibitor use and delayed access to care can increase severity.
A previous mild reaction does not guarantee a future reaction will be mild; ask specifically about previous airway or shock symptoms.

Clinical patterns

Mild allergic reaction

Localised itching, flushing, sneezing, mild nasal symptoms, limited urticaria or mild gastrointestinal discomfort without airway, breathing or circulation compromise. Observe closely because progression is possible.

Urticaria

Transient, raised, itchy wheals that migrate and fade, usually within 24 hours at each site. Urticaria alone is not anaphylaxis, but it may accompany it.

Angio-oedema

Deeper swelling of lips, eyelids, tongue, face, hands, feet or genitalia. Hoarseness, drooling, stridor, tongue swelling or difficulty swallowing signals airway danger. ACE-inhibitor angio-oedema may occur without hives and responds less reliably to antihistamines.

Anaphylaxis

A rapidly developing, life-threatening reaction involving airway, breathing or circulation, often with skin/mucosal changes but sometimes without them. Gastrointestinal symptoms can be prominent after food exposure.

Anaphylaxis recognition criteria

Think anaphylaxis: sudden illness after a likely trigger plus airway compromise (tongue/throat swelling, hoarse voice, stridor), breathing problems (wheeze, bronchospasm, hypoxia, respiratory distress) or circulation problems (hypotension, collapse, confusion, faintness). Skin or mucosal features—hives, flushing, itching, swelling—support the diagnosis but are not required.

Two or more systems affected rapidly after exposure: skin/mucosa plus respiratory, cardiovascular or persistent gastrointestinal symptoms.
Acute hypotension or collapse after a known allergen, even without skin signs.
Severe bronchospasm after exposure in a patient with asthma, even without rash.

Immediate scene and first contact actions

Recognise the emergency, call for help and bring the resuscitation trolley, oxygen and defibrillator.
Remove the trigger if possible: stop an infusion, remove a stinger without squeezing the venom sac, stop food or medicine exposure.
Lay the patient flat with legs elevated; allow a patient with severe breathing difficulty to sit with legs extended, and place a pregnant patient on the left side. Never allow standing or walking.
Give intramuscular adrenaline into the anterolateral middle third of the thigh as soon as anaphylaxis is suspected. Do not delay for IV access or antihistamines.
Record time, dose and response. Repeat according to the local protocol—commonly after about five minutes if airway, breathing or circulation problems persist.
Transfer every anaphylaxis patient to an appropriate clinical setting for monitoring, even if symptoms improve.

ABCDE emergency assessment

A — Airway

Look for tongue/lip swelling, hoarseness, stridor, drooling, inability to swallow or a muffled voice.
Call anaesthesia/airway help early. Prepare suction, oxygen, bag-mask ventilation and a difficult-airway plan.
Airway swelling can progress after initial improvement; reassess repeatedly.

B — Breathing

Assess respiratory rate, work, wheeze, silent chest, SpO2, cyanosis and ability to speak.
Give high-concentration oxygen for hypoxaemia or severe reaction and use bronchodilator therapy for persistent bronchospasm after adrenaline.
Be alert for upper-airway obstruction, pulmonary oedema, aspiration and fatigue.

C — Circulation

Check pulse, blood pressure, capillary refill, mental state, skin temperature and urine output.
Establish IV or IO access, obtain ECG and give warmed isotonic crystalloid boluses for shock with repeated reassessment.
If shock persists after IM adrenaline and fluids, call critical care for an adrenaline infusion; IV adrenaline is for experienced specialists with continuous monitoring.

D — Disability

Assess GCS/AVPU, glucose, agitation, collapse and seizure activity.
Confusion or drowsiness can indicate cerebral hypoperfusion or hypoxia.

E — Exposure

Inspect skin, mucosa, injection sites, stings and medical devices; look for urticaria, flushing, pallor or angio-oedema.
Prevent heat loss and examine for alternative causes such as sepsis, asthma, pulmonary embolism or vasovagal syncope.

Adrenaline: first-line treatment

Intramuscular adrenaline (epinephrine) is the life-saving first-line drug for anaphylaxis. Use the concentration and age/weight-based dose in the current local protocol. A commonly used professional reference is 1 mg/mL (1:1000) IM into the anterolateral thigh—adult dose often 0.5 mg and child dose approximately 0.01 mg/kg up to the local maximum. Repeat after about five minutes when airway, breathing or circulation problems persist. There is no absolute contraindication to IM adrenaline in life-threatening anaphylaxis.

Safety: Confirm the ampoule concentration, calculate the dose aloud, use the anterolateral thigh, record the exact time, and never delay adrenaline while trying to obtain IV access. IV bolus adrenaline from a 1:1000 ampoule is dangerous and must not be used outside an expert, monitored critical-care setting.

Adjunctive treatment after adrenaline

Oxygen: give high concentration for hypoxia, shock or severe respiratory symptoms; titrate once stable.
Fluids: give rapid isotonic crystalloid boluses in hypotension or poor perfusion, reassessing lungs, blood pressure and capillary refill.
Bronchodilator: inhaled salbutamol for persistent bronchospasm after adrenaline; do not use it instead of adrenaline.
Antihistamine: may relieve itch and hives after stabilisation, but does not treat airway swelling, bronchospasm or shock and must never delay adrenaline.
Corticosteroid: not a first-line resuscitation medicine; consider only under senior/local guidance for refractory asthma or selected reactions.
Glucagon: specialist advice may be needed for refractory anaphylaxis in a patient taking a beta-blocker.

Refractory anaphylaxis and cardiac arrest

Confirm the diagnosis, correct positioning and repeat IM adrenaline at the protocol interval.
Call critical care, obtain IV/IO access, give cautious crystalloid and identify ongoing exposure.
Start a titrated adrenaline infusion only with an experienced clinician, infusion pump and continuous ECG, blood-pressure and oxygenation monitoring.
Use advanced airway and ventilation support if needed; prepare for a difficult airway with swelling.
If cardiac arrest occurs, start high-quality CPR and follow the local ALS algorithm; give IV/IO adrenaline according to cardiac-arrest protocol, not the IM anaphylaxis dose.

Special situations

Pregnancy: treat maternal anaphylaxis promptly; place left lateral or manually displace the uterus and involve obstetric and neonatal teams.
Children: use weight-based dosing, age-appropriate equipment, maintenance fluids and early paediatric support.
Asthma: wheeze after allergen exposure should be treated as anaphylaxis until proven otherwise; adrenaline comes before inhalers.
ACE-inhibitor angio-oedema: stop the drug, assess the airway early and involve anaesthesia; absence of hives does not make it safe.
Venom sting: remove the stinger if visible, treat anaphylaxis, observe for recurrence and refer for venom immunotherapy assessment when indicated.
Infusion or transfusion reaction: stop the product, maintain IV access with compatible fluid, notify the blood bank/team and follow the transfusion-reaction pathway.

Differential diagnosis

Mimic	Clues	What prevents a dangerous error
Vasovagal syncope	Pallor, sweating, slow pulse and rapid improvement when supine; no wheeze or angio-oedema.	Lay flat, reassess ABCDE and give adrenaline if anaphylaxis features develop.
Acute severe asthma	Wheeze and bronchospasm without trigger-related multisystem features.	If allergen exposure or shock is present, treat as anaphylaxis first.
Panic attack	Hyperventilation and tingling without objective airway, breathing or circulation compromise.	Measure observations and do not dismiss a genuine allergic reaction.
Sepsis	Fever, infection source and progressive physiological derangement over hours/days.	Search for infection while treating immediate airway/breathing threats.
Hereditary angio-oedema	Recurrent swelling without urticaria, family history and abdominal attacks.	Early airway planning and specialist therapy; adrenaline may be less effective.
Drug rash/SJS-TEN	Delayed painful rash, blistering and mucosal erosions rather than minutes-to-hours collapse.	Stop culprit and manage as dermatological emergency; do not label all rashes anaphylaxis.

Investigations and observation

Diagnosis is clinical; do not delay treatment for tests.
Obtain ECG, glucose, electrolytes, blood gas/lactate and other tests according to severity and differential.
Serum tryptase may support later specialist investigation when collected at the protocol-defined times; a normal result does not exclude anaphylaxis.
Observe in a monitored setting. Longer observation or admission is appropriate after repeated adrenaline, severe respiratory/circulatory compromise, delayed presentation, asthma, mast-cell disease, uncertain trigger or poor access to emergency care.
Watch for biphasic reactions—recurrent symptoms after initial resolution without a new exposure.

Nursing interventions

Record time of onset, suspected trigger, ABCDE findings, adrenaline dose/time/site and response.
Keep the patient supine or in the safest breathing position, never allow unaided standing, and reassure continuously.
Monitor ECG, SpO2, respiratory rate, blood pressure, mental state, capillary refill and urine output.
Prepare repeated adrenaline, oxygen, suction, nebuliser, IV fluids, airway equipment and defibrillator.
Check all medicines for duplicate or hidden allergens and document adverse reactions prominently.
Provide privacy, explain procedures and support the family without delaying resuscitation.
Before discharge, teach auto-injector technique, trigger avoidance, emergency action plan and the need to call for help after use.

Observation, discharge and follow-up

Before discharge	Minimum safety check
Symptoms	Airway, breathing, circulation and skin/mucosal symptoms have fully resolved or are clearly improving.
Trigger	Likely trigger documented; ongoing exposure stopped; medicine and allergy record updated.
Education	Written action plan, trigger avoidance, emergency numbers and clear return precautions.
Equipment	Prescribed adrenaline auto-injector(s) where indicated, with demonstration and expiry advice.
Referral	Allergy/immunology or specialist review arranged for severe, recurrent, drug-, food- or venom-triggered reactions.
Support	Patient understands not to drive or walk alone if symptoms recur and knows when to call emergency services.

Prevention and patient education

Provide a written emergency plan describing symptoms, adrenaline use and when to repeat it or call for help.
Teach avoidance of the identified food, medicine, venom or latex and how to read labels or communicate the allergy.
Carry two adrenaline auto-injectors when prescribed, check expiry dates and store them according to manufacturer guidance.
Tell every healthcare worker about the reaction; wear a medical-alert card or bracelet.
Refer for supervised allergy testing, venom immunotherapy or drug-allergy assessment when appropriate.
Review asthma control and other co-factors that increase risk.

Scenario-based application

Scenario 1 — food-triggered anaphylaxis: Minutes after eating, a patient develops widespread hives, hoarse voice, wheeze and dizziness. Lay flat, call for help, give IM adrenaline in the lateral thigh immediately, give oxygen, obtain access and prepare fluids and a repeat dose. Antihistamine alone is unsafe.

Scenario 2 — anaphylaxis without a rash: After an injection, a patient becomes hypotensive, confused and breathless but has no hives. Treat as anaphylaxis based on airway/breathing/circulation compromise, give IM adrenaline and investigate other causes in parallel. Skin signs are not mandatory.

Scenario 3 — angio-oedema: A patient taking an ACE inhibitor has rapidly enlarging tongue swelling and a muffled voice. Stop the drug, call anaesthesia, prepare a difficult-airway plan, monitor continuously and give treatment under the local angio-oedema/anaphylaxis pathway. Do not wait for complete obstruction.

Scenario 4 — persistent shock: A patient remains hypotensive after two IM doses and fluid boluses. Confirm positioning and ongoing exposure, call critical care, start a specialist-titrated adrenaline infusion with continuous monitoring and prepare advanced airway/ALS support.

Common errors to avoid

Waiting for a rash, laboratory result or specialist review before giving IM adrenaline.
Allowing a recovering patient to stand or walk, causing sudden cardiovascular collapse.
Using antihistamines or steroids as substitutes for adrenaline.
Giving a dangerous IV adrenaline bolus from a 1:1000 ampoule outside expert critical care.
Failing to repeat adrenaline when airway, breathing or circulation problems persist.
Missing anaphylaxis in asthma, pregnancy, children, dark skin or patients without urticaria.
Discharging without an action plan, trigger documentation, auto-injector teaching and referral.

Documentation checklist

Time, trigger, route of exposure and previous allergic reactions.
ABCDE findings, vital-sign trends, skin/mucosal features and differential diagnosis.
Adrenaline concentration, dose, route, site, time and response; fluids, oxygen and adjuncts.
Airway/critical-care calls, observation period, investigations and disposition.
Allergy alert, pharmacovigilance report, action plan, device teaching and follow-up.

Quick revision questions

What is the difference between urticaria, angio-oedema and anaphylaxis?
Can anaphylaxis occur without skin signs? Explain.
What is the first-line medicine, route and preferred injection site?
How should a patient with anaphylaxis be positioned, and why must they not stand?
When should IM adrenaline be repeated?
Which treatments are adjuncts and must never replace adrenaline?
When is an adrenaline infusion appropriate?
What education and equipment are required before discharge?

Key takeaways

Anaphylaxis is a clinical diagnosis and may occur without hives.
Give IM adrenaline early into the anterolateral thigh; do not delay for tests or IV access.
Keep the patient safely positioned, give oxygen and fluids as indicated, and reassess continuously.
Antihistamines and steroids are adjuncts; they do not reverse shock or airway obstruction.
Every survivor needs observation, a written action plan, trigger documentation and specialist follow-up.

Burns: Emergency Recognition, Resuscitation, Wound Care and Referral

Why this matters to emergency medicine students: A burn is both a local tissue injury and a systemic emergency. Heat, chemicals, electricity, radiation or friction can destroy the skin barrier, cause airway injury, produce shock, release toxic gases, damage muscle and bone, and create lifelong scarring or disability. Good first aid limits tissue damage; disciplined ABCDE assessment identifies hidden threats; accurate depth and total-body-surface-area (TBSA) estimation guides fluids and referral. Always follow the current Uganda Clinical Guidelines, local burns protocol and specialist advice for exact fluid rates, dressings, analgesia and transfer.

Learning objectives

Explain burn mechanisms, depth, extent and factors that determine severity.
Perform scene safety, first aid and an ABCDE primary survey, including inhalation and electrical injury assessment.
Estimate burn size and depth, start safe resuscitation and recognise when the patient needs a burns centre.
Provide pain relief, wound protection, tetanus care, infection prevention, nutrition and nursing monitoring.
Anticipate airway compromise, compartment effects, shock, hypothermia, renal injury and other complications.
Plan discharge, rehabilitation, scar prevention, psychosocial support and prevention education.

Definition and mechanisms

A burn is tissue damage caused by thermal energy, chemicals, electricity, radiation or intense friction. Thermal burns may be due to flame, hot liquid (scald), steam, hot object or explosion. Chemical burns continue to damage tissue until the agent is removed or diluted. Electrical burns may have tiny skin marks but deep muscle, nerve, vessel and cardiac injury. Inhalation injury can occur from smoke, hot gases or toxic products even when the skin burn is small.

Depth of burn

Depth	Typical appearance and sensation	Healing and emergency meaning
Superficial	Red, dry, blanching, painful; no blisters and intact epidermis.	Usually heals without a scar, but extensive area may still require assessment.
Superficial partial thickness	Moist, red, blistered, blanching and very painful.	Often heals within about two weeks with appropriate care; infection or delayed healing increases scarring.
Deep partial thickness	Pale or mottled, less blanching, drier and less painful as nerves are injured.	May take longer than two weeks and often needs specialist review or grafting.
Full thickness	White, brown, leathery or charred; dry and insensate centrally.	Cannot re-epithelialise reliably; requires urgent burns/surgical assessment.
Deep tissue injury	Extends into fat, muscle, tendon or bone; may be charred or waxy.	Threatens limb and life; requires surgery, resuscitation and specialist reconstruction.

Burn depth can evolve during the first 48 hours because of oedema, thrombosis, infection and inadequate perfusion. Reassess rather than relying on the first visual description.

Estimating extent and severity

Rule of nines: a rapid adult estimate that assigns approximate percentages to body regions; use the locally taught chart.
Lund–Browder chart: more accurate for children because body proportions change with age.
Patient’s palm: the patient’s palm including fingers is approximately 1% TBSA and is useful for small or scattered burns.
Count partial- and full-thickness areas; do not count simple erythema without epidermal injury in formal resuscitation estimates.
Record depth, TBSA, location, mechanism, time, associated injuries and whether the burn is circumferential.

High-risk burns: face, eyes, ears, hands, feet, genitalia, perineum, major joints, circumferential limbs or chest, deep/full-thickness burns, significant TBSA, inhalation injury, electrical or chemical burns, burns in children or frail adults, and burns with trauma, pregnancy or major comorbidity.

Scene safety and first contact

Ensure the scene is safe: stop flames, isolate electricity, ventilate smoke and use PPE for chemicals or contaminated clothing.
Stop the burning process. Remove the patient from the source; extinguish flames with stop–drop–roll, water or a suitable blanket when safe.
Remove hot, wet or contaminated clothing and jewellery, but do not pull off material stuck to the skin.
Cool thermal burns with cool running water for about 20 minutes as soon as possible; avoid ice, very cold water, butter, toothpaste, oils and powders.
For chemical burns, brush off dry powder first if safe, remove contaminated clothing and irrigate with copious water. Protect rescuers and bring the container or label.
Cover with a clean non-fluffy cloth or sterile dressing, keep the rest of the patient warm and arrange urgent transport for significant burns.

ABCDE primary survey

A — Airway and cervical spine

Look for facial burns, soot, singed nasal hair, hoarseness, stridor, carbonaceous sputum, oral oedema, drooling or difficulty swallowing.
Ask about enclosed-space fire and loss of consciousness; suspect inhalation injury even when the mouth appears normal.
Give high-flow oxygen when smoke inhalation or carbon monoxide exposure is suspected and involve anaesthesia early.
Airway oedema can worsen rapidly after fluid resuscitation; prepare for early controlled intubation if signs progress.
Maintain cervical-spine precautions when there was a fall, explosion or trauma.

B — Breathing

Assess respiratory rate, work, chest excursion, SpO2, wheeze, crackles and fatigue.
Carbon monoxide can make pulse oximetry falsely reassuring; use co-oximetry where available and rely on history, mental state and clinical signs.
Consider toxic smoke exposure, bronchospasm, pulmonary oedema and airway sloughing; prepare ventilatory support.
A tight circumferential chest burn can restrict expansion and may need urgent surgical assessment for escharotomy.

C — Circulation

Check pulse, blood pressure, capillary refill, skin temperature, peripheral pulses and ECG.
Insert two large-bore IV lines through unburned skin when possible; intraosseous access may be needed in shock if IV access fails.
Major burns cause capillary leak and hypovolaemia. Begin warmed isotonic crystalloid using the local burns formula when indicated and titrate to perfusion and urine output.
Control associated bleeding, remove constrictive items and reassess limb perfusion in circumferential injuries.

D — Disability

Assess GCS/AVPU, glucose, pupils, pain and evidence of head injury, hypoxia or poisoning.
Confusion, headache, seizures or collapse after smoke exposure may indicate carbon monoxide or cyanide toxicity.

E — Exposure and environment

Expose the whole patient to identify hidden burns and trauma, then cover promptly to prevent hypothermia.
Inspect the back, scalp, perineum, folds and pressure points; remove wet clothing and record burn time and mechanism.

Inhalation injury and toxic exposure

Upper-airway injury: progressive oedema, hoarse voice, stridor, drooling and difficulty swallowing. Early anaesthetic airway planning is safer than late rescue intubation.
Lower-airway injury: cough, wheeze, soot, bronchospasm, hypoxia and respiratory failure may evolve over hours.
Carbon monoxide: headache, dizziness, confusion, syncope, myocardial ischaemia or unexplained acidosis. Give high-concentration oxygen and consult toxicology/critical care.
Cyanide: consider in enclosed-space fire with severe lactic acidosis, cardiovascular collapse or altered mental state; seek urgent antidote advice under local protocol.
Do not use a normal SpO2 alone to exclude smoke toxicity.

Fluid resuscitation

Formal IV resuscitation is generally required for larger burns, commonly around 20% TBSA in adults and lower thresholds in children or vulnerable patients, according to local protocol. A commonly taught Parkland-style estimate is 4 mL of balanced crystalloid × body weight (kg) × %TBSA, with half in the first eight hours from the time of burn and the remainder over the next 16 hours. This is only a starting estimate—not a prescription. Children also need maintenance fluid, and all patients require titration to clinical response.

Calculate from the time of injury, subtract fluid already given and record the calculation clearly.
Use warmed balanced crystalloid where recommended; avoid hypothermia.
Monitor urine output hourly, mental state, pulse, blood pressure, capillary refill, lactate, electrolytes, pulmonary signs and limb perfusion.
Too little fluid causes shock and kidney injury; too much causes pulmonary oedema, abdominal compartment effects and worsening limb/chest pressure.
Escalate to a burns/critical-care team when targets are not achieved or large volumes are required.

Pain and anxiety management

Assess pain before and after cooling, dressing changes, transfer and procedures.
Use titrated IV or oral analgesia appropriate to severity, with respiratory and sedation monitoring.
Consider procedural analgesia or sedation for debridement and dressing changes only with trained staff and full monitoring.
Explain each procedure, involve a support person when appropriate and address fear, guilt and distress.
Do not inject into burned tissue, and do not allow pain relief to replace repeated neurovascular and respiratory assessment.

Wound care in the emergency department

After cooling and stabilisation, gently remove loose contaminants and cover with a clean, non-adherent dressing.
Do not break intact blisters routinely outside a specialist plan; remove devitalised tissue when indicated by trained clinicians.
Use sterile saline or an approved cleaning solution; avoid harsh scrubbing and household remedies.
Elevate burned limbs and protect exposed tendons, digits and pressure points.
Apply topical antimicrobial or advanced dressings only according to local burns protocol and allergy check.
Give tetanus vaccination or immunoglobulin according to wound status and immunisation history.
Systemic antibiotics are not used routinely as prophylaxis; use them for documented infection, sepsis or specialist-directed indications.

Special burn mechanisms

Chemical burns

Protect staff, remove contaminated clothing and brush off dry powder before irrigation.
Irrigate copiously with water; continue until pain and tissue pH improve according to local protocol. Do not attempt neutralisation with another chemical.
Ocular chemical injury is an emergency: irrigate immediately, check pH repeatedly and obtain ophthalmology review.
Hydrofluoric acid requires urgent calcium therapy advice because systemic hypocalcaemia and dysrhythmia can occur even with a small surface burn.

Electrical burns

Do not touch the patient until the power source is isolated.
Perform ECG and monitor for dysrhythmia; assess entry and exit wounds, tetany, falls, spinal injury and deep muscle damage.
Check urine colour and renal function for rhabdomyolysis; dark urine, severe swelling or rising potassium requires urgent escalation.

Radiation and friction

Remove the source, follow radiation-safety procedures and seek specialist advice.
Friction burns may conceal contamination and deeper tissue injury; clean carefully and assess for associated trauma.

Circumferential burns and escharotomy

A non-elastic full-thickness eschar can act like a tourniquet. Circumferential limb burns may compromise pulses and nerves; circumferential chest burns may restrict ventilation. Check pulses, Doppler signals, capillary refill, sensation, motor function and ventilatory pressures repeatedly. Urgent specialist assessment is required; escharotomy is a surgical procedure and should not be attempted by untrained staff.

Investigations

Serial full blood count, electrolytes, urea/creatinine, glucose, lactate and blood gas in significant burns.
Carboxyhaemoglobin/co-oximetry when carbon monoxide is suspected; do not rely on standard pulse oximetry.
ECG and cardiac monitoring for electrical injury, chest symptoms, syncope or significant systemic illness.
Chest imaging and bronchoscopy based on inhalation symptoms and specialist assessment.
Creatine kinase, urine myoglobin and potassium when electrical injury, crush injury or rhabdomyolysis is suspected.
Pregnancy test when relevant; imaging and analgesia should be planned safely.
Photographs, TBSA charting and serial measurements support referral and reassessment.

Nutrition and metabolic support

Large burns produce a hypermetabolic, catabolic response and increased protein loss.
Start oral or enteral nutrition early when safe; involve dietetics for high-calorie, high-protein planning.
Monitor glucose, electrolytes, weight, bowel function, wound healing and micronutrient needs.
Prevent nausea, constipation and aspiration; assess swallowing when facial or airway injury is present.

Referral and admission criteria

Refer/admit urgently when	Examples
Extent or depth	Large TBSA, deep partial/full-thickness or burns requiring formal fluid resuscitation.
Critical locations	Face, eyes, ears, hands, feet, genitalia, perineum or major joints.
Mechanism	Inhalation, chemical, electrical, radiation, explosion or associated trauma.
Patient factors	Children, frail adults, pregnancy, diabetes, immunosuppression or unreliable follow-up.
Complications	Shock, hypoxia, carbon monoxide/cyanide concern, circumferential injury, neurovascular compromise or uncontrolled pain.

When transferring, send the TBSA/depth estimate, photographs if policy permits, mechanism, time of injury, cooling duration, airway findings, fluids given, urine output, analgesia, tetanus status and all investigations.

Nursing interventions and monitoring

Record observations at the acuity-appropriate frequency and trend rather than relying on one set of vital signs.
Maintain strict input/output, hourly urine output in major burns and accurate fluid-balance charts.
Inspect dressings, drainage, colour, odour, pain, temperature and signs of infection.
Check peripheral pulses, sensation, movement and capillary refill in circumferential or limb burns.
Maintain warmth while avoiding overheating, pressure injury and dehydration.
Administer analgesia and antiemetics safely; pre-medicate for dressing care.
Use aseptic line and wound care, hand hygiene and safe disposal of contaminated material.
Support nutrition, sleep, communication, mobility and psychological wellbeing.
Document depth, TBSA, photographs/measurements, dressings, response and every escalation.

Complications

Airway obstruction, inhalation pneumonitis, carbon monoxide or cyanide poisoning and respiratory failure.
Burn shock, hypothermia, electrolyte abnormalities, acute kidney injury and rhabdomyolysis.
Infection, sepsis, pneumonia, wound conversion and delayed healing.
Compartment effects, limb ischaemia, contractures and functional loss.
Hypertrophic scars, keloids, itch, chronic pain, pigment change and psychological trauma.
Malnutrition, anaemia, venous thromboembolism and pressure injuries during prolonged admission.

Discharge and rehabilitation

Give written wound-care instructions, dressing schedule, analgesia plan and clear return precautions.
Arrange review of burns that are deep, not healing as expected, infected, painful or functionally important.
Teach range-of-motion exercises and refer for physiotherapy/occupational therapy early when joints are involved.
Use pressure garments, silicone, moisturisers and sun protection only as prescribed by the burns team.
Address body image, sleep, trauma, school/work disruption and family support.
Ensure tetanus, nutrition, diabetes and smoking cessation needs are addressed.

Prevention

Keep hot liquids away from children, turn saucepan handles inward and test bath water.
Install safe cooking and electrical practices, maintain fire extinguishers and plan escape routes.
Store chemicals in labelled containers, never in drink bottles, and use gloves and eye protection.
Teach stop–drop–roll, smoke alarm response and safe handling of paraffin, gas and generators.
Use workplace PPE and lockout procedures for electrical, chemical and thermal hazards.

Scenario-based application

Scenario 1 — scald: A child spills hot tea over the chest and arm. Remove clothing not stuck to skin, cool under running water for about 20 minutes while keeping the child warm, cover loosely, assess ABCDE and TBSA, give analgesia and arrange paediatric/burns assessment. Do not apply toothpaste or ice.

Scenario 2 — enclosed-space fire: An adult rescued from a smoky room is confused, hoarse and tachycardic with a normal pulse oximeter reading. Give high-concentration oxygen, prepare for early airway control, assess for carbon monoxide/cyanide toxicity, obtain ECG/co-oximetry where available and transfer to critical care. A normal SpO2 does not exclude carbon monoxide poisoning.

Scenario 3 — circumferential limb burn: A patient with a full-thickness forearm burn develops increasing pain, numb fingers and weak Doppler signals. Elevate and reassess neurovascular status, obtain urgent burns/surgical review and prepare for specialist escharotomy. Do not wrap tightly or delay for routine imaging.

Scenario 4 — electrical injury: A worker touched a live cable and has small entry/exit wounds. Isolate power, perform ABCDE, ECG and cardiac monitoring, assess for falls and deep muscle injury, check renal markers and urine, and refer even if the skin area appears small.

Common errors to avoid

Cooling with ice or very cold water and causing hypothermia or further tissue injury.
Applying butter, toothpaste, oils, powders or unknown herbal preparations.
Pulling away clothing stuck to the wound or using adhesive dressings on burned skin.
Underestimating TBSA, inhalation injury, electrical depth or chemical continuation.
Giving large unmonitored fluid volumes or failing to calculate from time of injury.
Using prophylactic antibiotics for every burn or ignoring infection and tetanus assessment.
Missing circumferential chest/limb compromise and declining perfusion.
Discharging a high-risk burn without specialist review and follow-up.

Documentation checklist

Mechanism, time, enclosed-space exposure, chemical/electrical source and first aid performed.
ABCDE findings, airway risk, oxygen therapy, ECG, pain and mental status.
Depth, TBSA method, location, circumferential involvement, neurovascular status and photographs if permitted.
IV access, fluid calculation/rate, urine output, analgesia, tetanus and dressings.
Investigations, specialist calls, referral destination, handover and patient education.

Quick revision questions

What are the first five actions for a fresh thermal burn?
How do superficial, partial-thickness and full-thickness burns differ?
Which methods estimate TBSA, and why is Lund–Browder preferred in children?
What signs suggest inhalation injury and impending airway compromise?
When is formal IV fluid resuscitation required, and what clinical endpoints guide titration?
Why are electrical burns dangerous despite small skin wounds?
What burns require urgent specialist referral?
Which household remedies should never be applied to a burn?

Key takeaways

Stop the burning process, cool safely, cover gently and prevent hypothermia.
ABCDE comes before detailed wound care; airway and inhalation injury may be more dangerous than the visible burn.
Estimate depth and TBSA, calculate fluids from the time of injury and titrate to perfusion and urine output.
Electrical, chemical, inhalation, circumferential and critical-site burns need early specialist input.
Pain control, aseptic wound care, nutrition, rehabilitation and prevention determine long-term outcome.

Toxic Epidermal Necrolysis: Recognition, Resuscitation and Emergency Management

Toxic Epidermal Necrolysis (TEN): Recognition, Resuscitation and Emergency Management

Why this is an emergency: Toxic epidermal necrolysis (TEN) is a rare, life-threatening mucocutaneous reaction, usually to a medicine, in which widespread keratinocyte death causes painful epidermal detachment and loss of the skin barrier. The patient behaves physiologically like a major burn: fluid and heat are lost, infection risk rises, mucosal surfaces may obstruct eating, breathing, urination and vision, and rapid organ failure can occur. Immediate withdrawal of the suspected culprit and expert multidisciplinary supportive care are the priorities. Exact treatment decisions must be made with dermatology, critical-care, burns and ophthalmology teams using current local protocols.

Learning objectives

Define TEN and place it on the Stevens–Johnson syndrome (SJS) spectrum.
Recognise the prodrome, painful rash, epidermal detachment and multisite mucosal disease.
Perform an ABCDE assessment while protecting the airway, skin barrier, eyes, fluids and temperature.
Identify culprit medicines, stop unsafe exposures and document a permanent severe drug reaction.
Use a structured approach to fluids, wound care, analgesia, nutrition, infection surveillance and organ support.
Explain when to transfer to ICU/burns care and how to prevent long-term ocular, genital, pulmonary and psychological complications.

Definition and SJS–TEN spectrum

SJS and TEN are severe, immune-mediated epidermal necrolysis syndromes. They are classified by the percentage of detached or detachable body-surface area (BSA): SJS is generally less than 10%, SJS–TEN overlap is 10–30%, and TEN is more than 30%. The cutaneous percentage does not fully describe severity because small areas with extensive mucosal disease can threaten the airway, eyes, nutrition and urine flow. A positive Nikolsky sign (epidermis shearing with gentle pressure) may occur, but forceful rubbing is unsafe.

The condition is not ordinary urticaria, a simple drug rash or an infection that can be managed with topical cream. It is a time-critical dermatological and resuscitation emergency and should be managed in hospital, preferably in a burns or intensive-care environment when extensive.

Causes and high-risk medicines

Most adult cases are medication-related. The reaction often begins one to four weeks after a new medicine, but it can occur sooner after re-exposure or later with some agents. Commonly implicated groups include:

Allopurinol.
Sulfonamide antibiotics, including co-trimoxazole, and other antibiotics.
Aromatic anticonvulsants such as carbamazepine, phenytoin, phenobarbital and lamotrigine.
Some non-steroidal anti-inflammatory drugs, particularly oxicam derivatives.
Nevirapine and other antiretroviral or immunomodulating medicines.
Other drugs, herbal preparations and combinations must be assessed individually; never assume an unfamiliar medicine is harmless.

Infections such as Mycoplasma pneumoniae and other triggers may produce a similar mucocutaneous syndrome, especially in younger people. Ask about recent infections, vaccines, cancer therapy, radiotherapy and herbal or traditional medicines.

Pathophysiology

Cytotoxic T-cell and natural-killer-cell responses injure keratinocytes through granulysin, perforin/granzyme and related pathways.
Widespread apoptosis causes full-thickness epidermal necrosis and separation at the dermoepidermal junction.
Loss of the epidermal barrier causes transepidermal water loss, hypothermia, pain, fluid and electrolyte disturbance and susceptibility to invasive infection.
Mucosal epithelial necrosis causes conjunctivitis and corneal injury, painful oral erosions, dysphagia, genital/urinary erosions and airway or respiratory complications.
Inflammatory mediators can produce renal, hepatic, pulmonary, cardiac and haematological organ dysfunction.

Early presentation and clinical progression

The first phase resembles a severe viral illness: fever, malaise, sore throat, cough, headache, myalgia, arthralgia and eye irritation. Within days, the patient develops skin pain and dusky erythematous or atypical targetoid macules, often on the trunk and face. Lesions coalesce, become flaccid blisters and peel, leaving raw, tender erosions. Mucosal involvement is common and may precede obvious skin detachment.

Skin: severe tenderness, dusky macules, flaccid bullae, epidermal detachment, erosions and a positive gentle-shear sign.
Eyes: red painful eyes, photophobia, discharge, blurred vision, conjunctival membranes or inability to open the eyes.
Mouth and throat: painful lips, haemorrhagic crusting, oral erosions, drooling, dysphagia and inability to drink.
Genital and urinary: erosions, dysuria, urinary retention, vaginal or urethral involvement.
Respiratory: cough, hypoxia, wheeze, bronchial sloughing or respiratory failure.
Systemic: tachycardia, fever or hypothermia, hypotension, dehydration, confusion and reduced urine output.

Recognition: red flags requiring immediate escalation

Suspect SJS/TEN and call senior help now when there is a new medicine plus fever and painful skin, dusky targetoid lesions, blistering or peeling, skin tenderness out of proportion to visible rash, or erosions at two or more mucosal sites. Escalate urgently for airway symptoms, ocular pain/vision change, extensive detachment, shock, hypoxia, inability to drink or pass urine, rapidly rising BSA, confusion or suspected sepsis.

Do not wait for a dermatology appointment, a positive culture or a complete laboratory panel before stopping a suspected culprit and arranging transfer.

Immediate contact and safety

Use standard precautions, hand hygiene and gentle handling; add eye and body protection if there is fluid leakage.
Place the patient in a warm, low-traffic area and minimise friction, adhesives and unnecessary transfers.
Ask the patient or family to bring all medicines, blister packs, traditional remedies and recent prescriptions.
Stop the suspected culprit immediately after a clinician review; stop non-essential medicines until the medication list is reconciled.
Do not restart, rechallenge or give a related high-risk drug without specialist advice.
Call dermatology, critical care/burns, ophthalmology and relevant surgical or urology/gynaecology teams early.

ABCDE assessment

A — Airway

Listen for hoarseness, stridor, muffled voice, drooling or inability to swallow.
Inspect oral and pharyngeal sloughing; ask about throat pain and aspiration.
Prepare suction, oxygen and difficult-airway equipment. Involve anaesthesia early because progressive mucosal oedema and sloughing can make later intubation hazardous.

B — Breathing

Measure respiratory rate, work of breathing, SpO2 and chest excursion; ask about cough or pleuritic pain.
Give oxygen for hypoxaemia, obtain blood gas or chest imaging when indicated, and consider bronchoscopic assessment for airway sloughing in critical care.

C — Circulation

Check pulse, blood pressure, capillary refill, peripheral temperature, mental status and urine output.
Establish IV access through intact skin where possible; take blood samples, group and cross-match if extensive, and culture when infection is suspected.
Replace fluid and electrolytes using careful reassessment rather than blindly applying a major-burn formula; TEN losses vary with detachment and urine output.

D — Disability

Assess GCS/AVPU, glucose, pain, delirium and anxiety.
Severe pain, hypoxia, sepsis, dehydration and opioid accumulation can all alter mental state.

E — Exposure

Expose gently, inspect the entire skin and all mucosal sites, estimate detached/detachable BSA and prevent heat loss.
Remove wet clothing and jewellery carefully; avoid adhesive ECG pads on denuded skin and use non-traumatic alternatives.

Focused history and medication reconciliation

History area	Questions and emergency relevance
Timeline	When did each medicine start, stop or change? When did fever, pain, rash and mucosal symptoms appear?
All products	Prescription, over-the-counter, antimalarial, antibiotic, anticonvulsant, ART, herbal, traditional, topical and recreational products.
Previous reaction	Any prior rash, allergy, hospitalisation or family history of severe drug reactions?
Mucosal function	Can the patient see, swallow, drink, urinate and breathe normally? These answers guide urgent specialist care.
Comorbidity	HIV, cancer, renal/liver disease, diabetes, pregnancy, epilepsy, malnutrition or immune suppression.
Exposure/infection	Recent respiratory illness, sick contacts, travel, vaccination or radiotherapy.

Record generic and brand names, dose, route, dates and indication. If several medicines were started together, do not guess the culprit: stop unnecessary drugs, seek expert review and report the suspected adverse reaction through the appropriate pharmacovigilance system.

Examination and estimating skin involvement

Describe lesion type, colour, tenderness, blistering, detachment and distribution. Document whether skin is intact, detachable or already denuded.
Estimate BSA using the patient’s palm including fingers as approximately 1% or a locally taught chart; record the method used.
Assess the mouth, eyes, nose, ears, genitalia and anus while protecting privacy.
Check for pressure injury, infection, purulence, malodour, necrosis, peripheral perfusion and joint movement.
Repeat the examination because detachment can progress after arrival.

DRUG-SKIN — Discontinue culprit; Resuscitate ABCDE; Urgently transfer; Gentle skin care; Scan mucosa; Keep warm, hydrated and monitored.

Differential diagnoses

Condition	Distinguishing clues	Immediate implication
Staphylococcal scalded skin syndrome	Usually children, superficial tenderness and positive Nikolsky but mucosa often spared.	Urgent paediatric/infectious-disease care; culture suspected focus.
Generalised bullous fixed drug eruption	Fewer sharply demarcated lesions, recurrent at same sites and less systemic illness.	Still stop culprit; specialist confirmation needed.
Erythema multiforme	Typical raised target lesions, often acral and less extensive detachment.	Assess mucosa and rule out SJS/TEN when severe.
Acute generalized exanthematous pustulosis	Numerous sterile pustules, neutrophilia and shorter course.	Stop culprit and monitor systemic complications.
Generalised drug eruption	Morbilliform rash without skin pain, detachment or major mucosal erosions.	May be less dangerous, but reassess if it evolves.
Burn or chemical injury	Exposure history and distribution matching contact; no typical drug latency.	Remove exposure and use burn protocol.
Necrotising infection	Severe focal pain, toxicity, gas or purulence rather than diffuse mucocutaneous necrolysis.	Urgent surgical review and antimicrobials.

Investigations and diagnosis

Full blood count, electrolytes, urea/creatinine, glucose, liver tests, bicarbonate and albumin.
Blood gas and lactate if shock, hypoxia or organ dysfunction is present.
Blood cultures and cultures of clinically infected sites; do not give prophylactic antibiotics simply because skin is denuded.
Urinalysis and urine culture if dysuria, retention or sepsis is suspected.
Chest radiograph, ECG and additional imaging guided by respiratory or organ symptoms.
Skin biopsy from a fresh lesion for histopathology and direct immunofluorescence when available; treatment should not wait for the report.
Use SCORTEN or the locally adopted prognostic tool within the first 24 hours and repeat at the recommended interval. It supports communication and escalation; it does not replace bedside judgement.

Immediate treatment priorities

Stop the suspected drug: the most important time-critical intervention.
Transfer: arrange admission to ICU, a burns unit or a specialist centre according to BSA, physiology and local capability.
Protect the barrier: use a warm environment, pressure-relieving surface, non-adherent dressings and gentle handling.
Control pain: titrate appropriate analgesia, monitor sedation and avoid unnecessary intramuscular injections through damaged skin.
Replace losses: give warmed fluids and electrolytes based on perfusion, urine output, serum results and ongoing loss.
Assess mucosa early: urgent ophthalmology for every patient with eye symptoms; assess mouth, airway, genital and urinary involvement.
Prevent secondary harm: avoid adhesive tape, friction, unneeded antibiotics, latex exposure and unreviewed medicines.

Skin and wound care

Use a warm room and a pressure-relieving mattress; minimise handling, shear and unnecessary dressing changes.
Clean gently with sterile saline or an approved non-irritating solution. Avoid vigorous scrubbing, alcohol and harsh antiseptics on denuded tissue.
Protect detached areas with non-adherent silicone or paraffin gauze and an appropriate secondary dressing; follow the burns/dermatology team’s method.
Leave stable epidermal roofs in place unless they are infected, non-viable or obstruct care; debride only with expert direction.
Elevate oedematous limbs, protect heels and reposition carefully.
Use aseptic technique, document drainage and inspect for increasing pain, pus, odour, necrosis or new systemic deterioration.

Fluid, electrolyte and temperature management

TEN patients lose fluid through damaged skin and may be unable to drink because of oral erosions. Over-resuscitation can cause pulmonary oedema, while under-resuscitation causes shock and kidney injury. Use warmed isotonic fluid, frequent reassessment and a urinary catheter only when indicated and managed aseptically.

Set a urine-output target with the senior team and monitor hourly in unstable or extensive disease.
Record all oral, IV, enteral and urinary losses; trend weight, oedema, sodium, potassium, bicarbonate, creatinine and albumin.
Correct electrolyte abnormalities gradually and safely; review renal function before nephrotoxic medicines.
Prevent hypothermia with a warm room, warmed fluids, blankets and minimal exposure time.
Review fluid needs whenever skin loss changes, fever rises, oral intake improves or organ function worsens.

Mucosal and organ-specific care

Eyes

Urgent ophthalmology assessment is required even when eye involvement looks mild.
Use prescribed preservative-free lubricants, regular inspection and specialist-directed topical therapy; watch for epithelial defects, symblepharon, ulceration and visual loss.
Do not forcibly open adhered eyelids or put unprescribed drops on a damaged cornea.

Mouth and nutrition

Assess swallowing, hydration, oral bleeding and airway protection.
Use gentle oral care, prescribed analgesic mouth preparations and soft, high-calorie foods or enteral feeding when safe.
Involve dietetics, speech/swallow specialists and anaesthesia if aspiration risk is present.

Genital and urinary tract

Inspect for erosions, retention, bleeding and adhesions with consent and a chaperone.
Seek urology or gynaecology input; catheterisation may be necessary for retention but must be gentle and aseptic.

Respiratory system

Monitor cough, oxygenation, voice, secretions and work of breathing. Sloughing can affect the tracheobronchial tree.
Escalate for bronchoscopy, ventilatory support or airway intervention when clinically indicated.

Pain, anxiety and psychological support

Assess pain at rest and during dressing changes; pre-medicate before procedures and use multimodal analgesia.
Monitor opioid effect, respiratory rate, sedation, constipation and renal/hepatic considerations.
Explain each touch and procedure, involve a trusted support person with consent and provide privacy.
Offer psychological support; fear, isolation, body-image change and sleep disruption are common.
Use physiotherapy and gentle range-of-motion exercises when medically safe to reduce contractures and pneumonia.

Infection prevention and treatment

Denuded skin is not automatically infected. Routine prophylactic systemic antibiotics are generally avoided because they select resistant organisms and can cause new drug reactions. Use meticulous hand hygiene, aseptic wound care, surveillance cultures only when indicated and prompt targeted therapy for clinical sepsis or a documented infection.

Monitor temperature, haemodynamics, mental state, wound appearance, white-cell count, lactate and organ function.
Look for increasing wound pain, purulence, malodour, cellulitis, respiratory infection, line infection or urinary infection.
Take cultures before antibiotics when feasible, but do not delay treatment in shock.
Use isolation according to local infection-prevention policy, especially if a transmissible infection is suspected.
Review every medicine for unnecessary antimicrobial exposure and allergy risk.

Specialist-directed immunomodulatory therapy

No single systemic medicine has universal evidence or replaces withdrawal of the culprit and high-quality supportive care. Dermatology and critical-care teams may consider corticosteroids, ciclosporin, intravenous immunoglobulin or other immunomodulators based on disease timing, contraindications, local expertise and available evidence. Explain uncertainty, monitor infection and organ function, and never delay transfer while debating a specialist therapy.

Nursing care plan

Problem	Goals	Core nursing actions
Impaired skin integrity	Protect tissue and support re-epithelialisation.	Warm environment, non-adherent dressings, aseptic technique, pressure relief and wound documentation.
Fluid/electrolyte loss	Stable perfusion, urine output and laboratory values.	Hourly input/output when indicated, daily weight, warmed fluids, laboratory trends and escalation of oliguria.
Severe pain	Comfort at rest and during care.	Regular pain scoring, pre-medication, gentle handling, prescribed analgesia and reassessment.
Risk of infection	Early recognition without unnecessary antibiotics.	Hand hygiene, aseptic lines/dressings, surveillance of wounds and rapid culture/escalation for sepsis.
Mucosal dysfunction	Maintain vision, airway, hydration, nutrition and urine flow.	Eye/oral/genital care as prescribed, swallow assessment, nutrition support and specialist referrals.

Complications

Hypovolaemic or distributive shock, acute kidney injury and electrolyte abnormalities.
Sepsis, pneumonia, bloodstream infection and multiorgan failure.
Airway obstruction, bronchial sloughing, hypoxaemia and respiratory failure.
Corneal ulceration, symblepharon, scarring, dry eye and permanent visual loss.
Oral strictures, malnutrition, genital adhesions, urethral stenosis and sexual dysfunction.
Thromboembolism, pressure injury, contractures, chronic pain, pigment change and post-traumatic stress.
Death; risk is related to age, extent, comorbidity, organ failure and delayed withdrawal of the culprit.

Transfer and escalation criteria

Any suspected TEN or SJS with progressive detachment requires hospital admission and specialist consultation.
Transfer to ICU/burns care for extensive BSA, shock, hypoxia, airway concern, severe mucosal disease, renal failure, altered mental state or rapidly worsening skin loss.
Arrange specialist eye assessment for any ocular symptom and surgical/urology/gynaecology review for urinary or genital obstruction.
Use a structured handover: culprit medicines and time, BSA, mucosae involved, airway, fluids, urine output, investigations, cultures, antibiotics and outstanding referrals.

Discharge, recovery and long-term follow-up

Provide written documentation naming the suspected culprit and related medicines to avoid; add an allergy alert to the medical record and advise a medical-alert card or bracelet.
Refer for ophthalmology follow-up even after eye symptoms improve; late scarring can appear after discharge.
Review skin healing, pain, pigmentation, itch, nutrition, mobility, genital/urinary function and psychological wellbeing.
Teach the patient to seek urgent care for fever, new blisters, eye pain, breathing difficulty, inability to drink or pass urine.
Report the suspected adverse drug reaction to the national pharmacovigilance system and communicate it to every future healthcare provider.

Scenario-based application

Scenario 1 — early recognition: A patient started co-trimoxazole 10 days ago and now has fever, skin pain, dusky trunk lesions, lip crusting and red eyes. Stop the suspected medicine, perform ABCDE, examine all mucosae, establish access, give supportive care and arrange urgent dermatology/burns/ophthalmology assessment. Do not discharge with an antihistamine alone.

Scenario 2 — shock and extensive detachment: A patient has 40% detached skin, tachycardia, hypotension, oliguria and confusion. Treat as a resuscitation emergency: warm environment, oxygen, IV access, carefully titrated warmed fluids, urine monitoring, analgesia, urgent ICU/burns transfer and early specialist airway planning. Do not use adhesive tape or rough handling.

Scenario 3 — ocular emergency: A stable patient has painful red eyes and photophobia with limited skin detachment. Arrange same-day ophthalmology review, use only prescribed eye care and document visual symptoms. Mild-looking skin disease does not make ocular involvement safe to ignore.

Common errors to avoid

Continuing the suspected culprit while waiting for a biopsy or specialist review.
Calling the condition a simple allergy despite skin pain, blistering or mucosal erosions.
Using routine prophylactic antibiotics on every denuded patient.
Underestimating fluid, heat and nutritional losses because the visible BSA seems small.
Applying adhesive dressings, vigorous debridement, alcohol or irritating antiseptics to fragile skin.
Missing eye, airway, urinary or genital disease.
Starting immunomodulatory therapy without specialist discussion or infection surveillance.
Failing to document and communicate the culprit drug, leading to dangerous re-exposure.

Documentation checklist

All medicines and products, start dates, suspected culprit and withdrawal time.
ABCDE findings, vitals, pain, mental state, glucose, BSA estimate and detached versus detachable skin.
Every mucosal site examined and specialist referrals made.
Fluids, urine output, electrolyte trends, analgesia, dressings, cultures and antibiotics.
SCORTEN or local severity assessment and transfer/handover details.
Adverse-drug-reaction report, allergy alert, patient education and follow-up plan.

Quick revision questions

How is TEN defined in relation to SJS and SJS–TEN overlap?
Which medication groups commonly trigger TEN?
What are the first three actions when TEN is suspected?
Why must eyes, mouth, airway and genital/urinary mucosa be assessed early?
Why is routine prophylactic antibiotic therapy discouraged?
What factors determine transfer to a burns or intensive-care unit?
What information must be written in the permanent drug-allergy record?
List five complications that may persist after the skin heals.

Key takeaways

TEN is a medical emergency, not a routine rash.
Stop the suspected culprit immediately and arrange specialist hospital care.
ABCDE, airway planning, warmed fluid/electrolyte care, analgesia and barrier protection save lives.
Ophthalmology, nutrition, wound, urinary, respiratory and psychological care are essential—not optional extras.
Prevent re-exposure by documenting, reporting and communicating the suspected medicine forever.

Cellulitis: Recognition, Assessment, Resuscitation and Emergency Management

Why this matters to emergency medicine students: Cellulitis is a bacterial infection of the dermis and subcutaneous tissue. It may look localised at first, yet rapidly progress to lymphangitis, bacteraemia, sepsis, deep-space infection, necrotising fasciitis or limb-threatening complications. The emergency practitioner must identify the uncomplicated patient who can receive prompt outpatient treatment, while recognising the patient who needs resuscitation, intravenous antibiotics, imaging, surgical review or admission. This guide follows the patient from first contact through discharge, reassessment and prevention. Antibiotic choices and doses must follow the current Uganda Clinical Guidelines, facility antibiogram, allergies, renal function and senior clinician advice.

Learning objectives

Define cellulitis and explain how bacteria enter and spread through skin and subcutaneous tissues.
Identify risk factors, common organisms, typical findings and early systemic deterioration.
Perform a structured primary survey and focused skin, limb and neurovascular examination.
Distinguish cellulitis from erysipelas, abscess, necrotising fasciitis, DVT, allergic inflammation, burns and other mimics.
Provide safe first aid, analgesia, wound care, sepsis treatment, antibiotic therapy and escalation.
Plan nursing monitoring, documentation, discharge education, follow-up and recurrence prevention.

Definition and clinical concept

Cellulitis is an acute, spreading infection involving the deeper dermis and subcutaneous tissue. The infected skin becomes inflamed because bacterial products and the host immune response cause vasodilation, capillary leakage, oedema and leukocyte migration. Erysipelas is a more superficial infection with a raised, sharply demarcated border; in practice the two can overlap. A cellulitis lesion is usually unilateral, warm, tender, swollen and progressively red, although erythema can be difficult to appreciate on dark skin. The diagnosis is primarily clinical; a negative culture does not exclude it.

Cellulitis is not the same as an abscess. An abscess is a localised collection of pus that usually requires incision and drainage, whereas non-purulent cellulitis is treated primarily with antibiotics and treatment of the entry site. A patient may have both conditions.

Causative organisms and pathophysiology

Beta-haemolytic streptococci (especially group A streptococcus) commonly cause non-purulent cellulitis and spread through lymphatics.
Staphylococcus aureus, including community-associated MRSA where prevalent, is more likely with purulence, penetrating trauma, abscesses or injection drug use.
Gram-negative and anaerobic organisms become more relevant in diabetic foot infection, chronic ulcers, perineal infection, immunosuppression, severe vascular disease, animal or human bites and water exposure.
Special exposures: Pasteurella after dog or cat bites, Capnocytophaga in a person with asplenia or severe alcohol use, Vibrio after seawater or raw seafood exposure, and Aeromonas after fresh-water exposure.

Bacteria usually enter through a breach in the protective barrier: cracked toe-web skin, tinea pedis, eczema, ulcers, injection sites, trauma, surgical wounds, burns, pressure injury or an unnoticed fissure. Lymphatic obstruction, oedema and poor perfusion reduce local clearance and increase recurrence.

Risk factors and vulnerable patients

Previous cellulitis or chronic lymphoedema.
Tinea pedis, nail disease, eczema, scabies excoriations or chronic dermatitis.
Diabetes mellitus, peripheral neuropathy, peripheral arterial disease or venous insufficiency.
Obesity, immobility, chronic leg oedema, heart failure or nephrotic syndrome.
Open wounds, ulcers, burns, pressure injuries, recent surgery or invasive devices.
Immunosuppression, HIV, chemotherapy, long-term corticosteroids or splenectomy.
Injection drug use, poor access to clean water, overcrowded living conditions or poor wound-care access.
Animal or human bites, penetrating injuries, aquatic exposure and recent travel.
Very young infants, older adults and pregnant patients may deteriorate with fewer local signs.

Typical presentation

Patients often report a progressively enlarging area of pain, warmth, swelling and redness over hours to several days. The border is usually poorly defined. Fever, chills, malaise, headache, myalgia, nausea and tender regional lymph nodes may occur. Lymphangitis appears as a red linear streak tracking proximally; lymphadenopathy may accompany it.

Inspect colour and compare with the opposite side; palpate for warmth, tenderness, oedema and induration.
Look for a portal of entry between toes, around nails, in a skin fold, at a wound or under a dressing.
Mark the edge with date and time or photograph according to policy; this helps judge progression.
Check for fluctuance, crepitus, bullae, dusky skin, skin anaesthesia, necrosis or pain beyond visible inflammation.
Examine the whole limb, not only the reddest area, and assess joints above and below.

Red flags for severe infection or a deeper emergency

Escalate immediately: hypotension, tachycardia with poor perfusion, altered mental status, respiratory distress, oliguria, rapidly spreading erythema, severe pain out of proportion, pain with passive movement, bullae, skin anaesthesia, dusky or violaceous skin, crepitus, haemorrhagic blisters, systemic toxicity, immunocompromise, facial or periorbital involvement, hand infection, genital/perineal involvement, infection over a prosthetic joint, or failure to improve after 48–72 hours of appropriate therapy.

These signs may indicate sepsis, an abscess, necrotising fasciitis, orbital cellulitis, septic arthritis, osteomyelitis, flexor tenosynovitis or another condition requiring urgent senior and surgical review. Do not wait for imaging when a time-critical surgical diagnosis is clinically suspected.

First contact and scene safety

Perform hand hygiene and wear gloves; add eye and body protection if drainage or splashing is possible.
Introduce yourself, confirm identity, obtain consent and provide privacy, especially when examining groin, breast, buttock or genital lesions.
Ask about onset, speed of spread, fever, rigors, pain severity, trauma, bites, water exposure, wounds, injections and previous antibiotics.
Ask about diabetes, HIV, steroid use, chemotherapy, vascular disease, lymphoedema, drug allergies, pregnancy and kidney or liver disease.
Do not squeeze, lance or massage a suspected abscess in the field. Cover an open wound with a clean dressing and avoid contamination.
Check vital signs early. Any abnormal physiology changes cellulitis from a simple skin problem into a possible sepsis pathway.

Primary survey: ABCDE approach

A — Airway

Assess speech, voice change, drooling, tongue or facial swelling and ability to handle secretions.
Facial, neck, dental or submandibular infection can threaten the airway; call senior airway help early.
Prepare suction, oxygen, airway equipment and a definitive-airway plan if swelling is progressing.

B — Breathing

Count respiratory rate, assess work of breathing, oxygen saturation, chest movement and mental state.
Give oxygen for hypoxaemia or shock according to local protocol; do not delay sepsis treatment while waiting for perfect observations.

C — Circulation

Check pulse, blood pressure, capillary refill, skin temperature, peripheral pulses and urine output.
Obtain IV access if the patient is systemically unwell; take blood samples and cultures before antibiotics only if this does not delay treatment.
For suspected sepsis or hypoperfusion, follow the facility sepsis bundle: cautious isotonic crystalloid, repeated perfusion assessment and early vasopressor/senior support when fluid-responsive shock is absent.

D — Disability

Assess AVPU or GCS, bedside glucose, pain score and new confusion.
Hypoglycaemia, severe sepsis, hypoxia and medication effects can coexist; treat immediately reversible threats.

E — Exposure and examination

Expose enough to inspect the entire skin surface while preventing heat loss and maintaining dignity.
Measure and mark the affected area, inspect wounds and folds, palpate for fluctuance and crepitus, and check neurovascular status.
Look at the feet, toe webs, nails, pressure points, sacrum and perineum; hidden portals are common.

Focused history

Question	Why it matters
When did it begin and how quickly is it spreading?	Rapid progression raises concern for necrotising infection or severe sepsis.
Is pain mild, severe or out of proportion?	Disproportionate pain suggests deeper tissue involvement.
Was there a wound, bite, injection, operation or water exposure?	Predicts organisms, need for tetanus and special antibiotic coverage.
Any fever, rigors, vomiting, confusion, reduced urine or breathlessness?	Identifies systemic infection and organ dysfunction.
Previous episodes, antibiotics or resistant organisms?	Guides recurrence prevention and empirical treatment.
Diabetes, HIV, steroids, chemotherapy, vascular disease or lymphoedema?	Increases severity, atypical organisms and admission risk.
Drug allergies, pregnancy, renal or hepatic disease?	Determines safe drug selection and dosing.

Focused examination and severity assessment

Local: temperature, colour, borders, tenderness, induration, oedema, fluctuance, drainage, bullae, necrosis and crepitus.
Regional: lymphangitis, lymph nodes, joint range of motion, tendon function and compartment firmness.
Neurovascular: pulses, capillary refill, sensation, motor function and pain on passive stretch.
Systemic: temperature, heart rate, blood pressure, respiratory rate, SpO2, mental state and urine output.
Host: hydration, nutrition, glycaemic control, perfusion, immune status and ability to take oral medication.

SKIN-MAP — Spread speed and systemic signs; Known risk factors; Inspect entry site and inflammation; Neurovascular check; Mark the border; Abscess/necrosis look; Plan antibiotics, review and prevention.

Important differential diagnoses

Condition	Clues that support it	Emergency implication
Abscess	Fluctuant, focal swelling, pus or central tenderness.	Needs drainage and culture; antibiotics alone may fail.
Necrotising fasciitis	Severe pain, rapid spread, toxicity, bullae, anaesthesia, crepitus or skin discoloration.	Immediate surgical consultation; do not delay for imaging.
Erysipelas	Raised, bright-red, sharply demarcated superficial border.	Antibiotic therapy; monitor for systemic illness.
DVT	Swelling and pain without marked warmth or skin entry site; risk of thrombosis.	Requires vascular assessment; avoid assuming every red leg is cellulitis.
Contact dermatitis or allergy	Itching, bilateral or geometric distribution, exposure history, little systemic illness.	Remove trigger; antibiotics are not automatically indicated.
Septic arthritis	Severe joint pain, restricted passive movement, effusion and fever.	Urgent aspiration/orthopaedic review.
Gout or pseudogout	Acute hot joint with crystal disease history.	Must exclude septic arthritis before anti-inflammatory-only treatment.
Venous stasis dermatitis	Chronic bilateral pigmentation, scaling and oedema.	Compression and skin care; avoid unnecessary antibiotics.

Investigations

Most mild, typical cellulitis does not require extensive testing. Investigate according to severity, host factors, site and diagnostic uncertainty.

Bedside glucose: essential in diabetes, altered mental state or severe infection.
Full blood count, CRP/ESR and renal/electrolyte profile: useful when systemic illness, admission or IV therapy is likely.
Lactate and blood gas: consider in shock, hypoperfusion or suspected sepsis; interpret with the whole clinical picture.
Blood cultures: obtain in severe systemic illness, immunocompromise, unusual exposure or suspected bacteraemia; yield is low in uncomplicated cases.
Wound or pus culture: collect from purulent material after cleaning; superficial swabs of intact cellulitic skin are often misleading.
Ultrasound: useful for an occult abscess, retained foreign body or venous thrombosis when clinically indicated.
Plain radiograph: consider foreign body, gas, bone involvement or severe diabetic foot infection.
CT or MRI: for deep-space infection, osteomyelitis or uncertain anatomy after senior review; never let imaging delay surgery in suspected necrotising fasciitis.

Immediate treatment and first aid

Place the patient in a safe position, keep them warm and provide reassurance.
Remove constrictive jewellery or clothing from a swollen limb, documenting what was removed.
Clean visible contamination gently with clean water or saline; cover open areas with a sterile non-adherent dressing.
Elevate an affected limb where tolerated to reduce oedema, while checking that elevation does not worsen pain or perfusion.
Give analgesia according to protocol, reassess pain and avoid masking deterioration.
Check tetanus status for wounds and arrange vaccination or immunoglobulin when indicated by local guidance.
Do not apply irritant chemicals, herbal preparations, tight bandages or unprescribed steroids.
Escalate immediately if red flags, systemic illness, facial/eye involvement, rapidly spreading infection or high-risk host factors are present.

Antimicrobial management

Antibiotics should cover the likely organisms and be started promptly when cellulitis is clinically diagnosed. Choice, dose and duration depend on local resistance patterns, infection severity, allergy, renal function, pregnancy, age, site and culture results. Document the indication, route, first dose time, allergy check and planned review.

Mild non-purulent cellulitis: an appropriate oral agent active against streptococci and susceptible staphylococci is commonly used according to Uganda/local protocol.
Moderate infection, failed oral therapy or inability to absorb: consider hospital assessment and parenteral therapy with step-down to oral treatment after clear clinical improvement.
Severe infection or sepsis: obtain cultures where feasible and start broad IV empiric therapy that covers streptococci, staphylococci and, when indicated, Gram-negative and anaerobic organisms. Review daily and narrow once results and clinical response are known.
Purulence or abscess: source control through incision and drainage is central; add antibiotic therapy when systemic illness, extensive disease, rapid progression, immunocompromise or difficult sites are present.
MRSA risk: consider prior MRSA, recent hospitalisation or antibiotics, penetrating trauma, injection drug use, recurrent abscess or local epidemiology.
Bites and water exposure: use exposure-specific coverage and seek microbiology or infectious-disease advice.

Stewardship rule: Do not continue broad-spectrum treatment simply because the redness takes time to fade. Cellulitis can remain red for several days after bacteria are controlled. Assess fever, pain, spread, function, perfusion and systemic status, then adjust treatment with the clinical team.

Surgical and procedural management

Drain every clinically significant abscess and send pus for culture when appropriate.
Remove foreign bodies, devitalised tissue, infected sutures or obstructing material after appropriate assessment.
Request urgent surgical review for suspected necrotising infection, compartment syndrome, septic arthritis, infected prosthesis, deep hand infection, periorbital/orbital disease or Fournier’s gangrene.
Do not perform blind bedside procedures near major vessels, the eye, hand tendon sheaths, genitalia or a prosthetic joint.
Use aseptic technique, local anaesthesia or procedural sedation only within the practitioner’s competence and monitoring capability.

Special anatomical situations

Face and periorbital skin: examine vision, eye movements, pupils and pain with movement. Proptosis, reduced vision, ophthalmoplegia, severe headache or toxic appearance suggests orbital involvement and requires emergency admission and specialist review.
Hand and fingers: assess tendon function, sensation, pulses and passive stretch. Kanavel signs or rapidly progressive swelling need hand-surgery review.
Foot and diabetes: assess pulses, sensation, ulcers, callus, depth, bone exposure and glucose. Consider osteomyelitis and multidisciplinary diabetic-foot care.
Perineum: pain, swelling, bullae, crepitus or systemic toxicity may be Fournier’s gangrene; urgent resuscitation and surgery are required.
Breast or postoperative site: assess for abscess, wound dehiscence, prosthetic infection and need for imaging or surgical drainage.

Sepsis and deterioration pathway

Cellulitis can trigger bacteraemia and septic shock, particularly in older adults, people with diabetes, immunosuppression or extensive infection. Reassess frequently rather than relying on a single reassuring temperature.

Recognise abnormal physiology: altered mental state, fast breathing, hypotension, weak pulse, mottling, cold extremities, low urine output or rising lactate.
Call for senior help and move the patient to an area capable of continuous monitoring.
Obtain IV access, blood tests and cultures if feasible without delaying antibiotics.
Give timely antimicrobials and carefully titrated crystalloid for hypoperfusion, reassessing lungs, blood pressure, capillary refill and urine output after each bolus.
Escalate for vasopressor and critical-care support if shock persists or fluid is unsafe.
Search for source-control needs: abscess, necrotising infection, infected device, septic joint or osteomyelitis.

Nursing interventions

Record baseline observations, pain score, mental state, lesion location, dimensions, photographs or border markings according to policy.
Repeat observations at the frequency required by acuity; report new fever, hypotension, confusion, tachypnoea, reduced urine or rapidly expanding erythema.
Administer antibiotics on time, check allergies, observe for anaphylaxis, document response and maintain IV access.
Elevate the limb, protect pressure points, change dressings aseptically and assess drainage, odour, colour and tissue viability.
Monitor intake, output, glucose and renal function, especially during sepsis or IV therapy.
Provide analgesia and non-pharmacological comfort; reassess effect rather than simply recording administration.
Support nutrition, hydration, mobility and safe toileting while preventing falls.
Explain the treatment plan, antibiotic adherence, warning signs and follow-up in the patient’s preferred language.
Use standard precautions and dispose of contaminated dressings safely; apply additional precautions if drainage is uncontrolled or another transmissible infection is suspected.

Monitoring response to treatment

Time point	What to assess	Action if worse
At arrival	ABCDE, sepsis screen, pain, lesion size, perfusion and portal of entry.	Resuscitate, escalate and consider admission.
After first treatment	Allergy, analgesic effect, vital-sign trend, IV access and antibiotic timing.	Stop offending drug and treat reaction; call senior help.
Within 6–24 hours for admitted patients	Spread, fever, perfusion, urine output, mental state, labs and wound appearance.	Review diagnosis, source control, cultures and antibiotic spectrum.
At 48–72 hours	Systemic improvement, pain, function and whether the border has stopped advancing.	Reassess for abscess, necrotising infection, resistant organism, wrong diagnosis or non-adherence.
At completion/follow-up	Healing, oedema, skin integrity, tinea, ulcers and recurrence risks.	Institute prevention plan and specialist referral if recurrent.

Admission and discharge decisions

Consider admission when

There is sepsis, haemodynamic instability, altered mental state or organ dysfunction.
Infection is rapidly progressive, extensive, bullous, necrotic or associated with severe pain.
There is facial/periorbital, hand, genital, deep foot, prosthetic-joint or postoperative involvement.
The patient is immunocompromised, pregnant, very young, frail, unable to take oral medicines or unable to manage wound care.
Oral treatment has failed, adherence is doubtful or reliable follow-up is unavailable.

Discharge only when appropriate

Vital signs are stable, pain is controlled and there is no concern for deep infection or sepsis.
The patient can drink, take medication, elevate/protect the area and return for review.
A written plan gives the antibiotic name, route, schedule, duration, adverse effects and what to do if a dose is missed.
A review appointment or safety-net contact is arranged, usually within 24–72 hours depending on severity.

Complications

Abscess, lymphangitis, lymphadenitis and recurrent cellulitis.
Bacteraemia, sepsis, septic shock and metastatic infection.
Necrotising fasciitis, myositis, pyomyositis or compartment syndrome.
Septic arthritis, osteomyelitis or infected prosthetic material.
Orbital cellulitis, cavernous sinus thrombosis or intracranial spread from facial infection.
Chronic lymphoedema, tissue damage, scarring and functional impairment.
Drug reactions, antibiotic-associated diarrhoea and antimicrobial resistance.

Prevention and recurrence reduction

Wash minor wounds with clean running water, remove visible dirt and cover with a clean dressing.
Treat tinea pedis and cracked toe webs; dry carefully between toes and change socks regularly.
Moisturise eczema-prone skin, avoid scratching and keep nails short.
Manage diabetes, oedema, venous disease and weight with the appropriate clinical team.
Use compression for chronic oedema only after arterial circulation is assessed and acute infection has settled.
Use protective footwear and gloves; avoid walking barefoot where injury risk is high.
Seek early care for painful, hot, swollen skin rather than applying irritants or delaying treatment.
For frequent recurrences, look for untreated tinea, ulcers, lymphoedema, venous disease or nasal staphylococcal carriage and discuss specialist prevention.

Scenario-based application

Scenario 1 — uncomplicated lower-leg cellulitis: A stable adult has unilateral warmth, tenderness and spreading redness after a cracked toe web, with normal blood pressure and no fluctuance. Mark the border, examine the foot and toe webs, treat with protocol-directed oral antibiotics and analgesia, provide elevation and arrange early review. Explain that redness may resolve slowly but spread, fever or deterioration requires urgent return.

Scenario 2 — cellulitis with sepsis: A patient with diabetes has a hot leg, rigors, respiratory rate 30/min, confusion and a weak pulse. Move to resuscitation, perform ABCDE, obtain IV access and cultures without delaying broad empiric antibiotics, give carefully reassessed fluids, monitor urine and request senior/critical-care review. Do not discharge because the skin lesion appears small.

Scenario 3 — cellulitis or necrotising fasciitis? A patient reports unbearable pain extending beyond a rapidly reddening area; the skin is dusky with bullae and the patient is hypotensive. Treat as necrotising infection until proven otherwise: resuscitate, give broad IV antibiotics and obtain immediate surgical review. Imaging must not delay exploration.

Scenario 4 — diabetic foot: A person with neuropathy has a plantar ulcer, foul drainage and spreading redness. Check glucose, pulses, sensation, depth and bone exposure; obtain appropriate cultures and imaging, start protocol-directed treatment and involve diabetic-foot, surgical and vascular teams. Off-load the foot and never rely on pain severity because neuropathy may hide serious disease.

Common errors to avoid

Calling every red, swollen leg cellulitis without considering DVT, venous stasis or contact dermatitis.
Failing to inspect the toe webs, wound, perineum, pressure areas or concealed portal of entry.
Waiting for laboratory confirmation before giving antibiotics to a septic patient.
Using antibiotics alone for a drainable abscess.
Delaying surgery because an imaging report is pending when necrotising infection is clinically likely.
Prescribing broad antibiotics without review, culture interpretation or a stop/step-down plan.
Ignoring renal function, allergy, pregnancy, drug interactions or local resistance patterns.
Discharging without a border mark, clear safety-netting and a follow-up plan.

Documentation checklist

Time of arrival, history, allergies, comorbidities and relevant exposure.
ABCDE findings, vital-sign trend, pain score, glucose and sepsis screening.
Exact site, measurements, border marking/photograph, wound description and neurovascular findings.
Differential diagnosis, investigations, cultures and senior/surgical discussions.
Drug, dose, route, time, indication, response and adverse effects.
Wound care, elevation, mobility, intake/output and patient education.
Disposition, review date, return precautions and responsible clinician.

Quick revision questions

How does cellulitis differ clinically from an abscess and from erysipelas?
Name six risk factors for cellulitis recurrence.
Which findings make you suspect necrotising fasciitis rather than uncomplicated cellulitis?
When are blood cultures, ultrasound or advanced imaging useful?
What are the first five actions for a patient with cellulitis and septic shock?
Why is source control important in purulent infection?
What features make facial, hand, perineal or diabetic-foot cellulitis high risk?
What information must be included in discharge safety-netting?

Key takeaways

Cellulitis is a clinical diagnosis, but the emergency task is to identify severity and exclude deeper disease.
Always assess the whole patient with ABCDE, not only the red skin.
Rapid spread, disproportionate pain, bullae, crepitus, anaesthesia, shock or toxicity demand urgent escalation.
Use antibiotics responsibly, drain abscesses, obtain source control and review response within a defined timeframe.
Good wound care, management of oedema and tinea, glycaemic control and clear follow-up prevent recurrence.

Necrotizing Fasciitis: Recognition, Resuscitation and Emergency Management

Why this topic matters: Necrotizing fasciitis is a rapidly progressive, life-threatening infection of fascia and deep soft tissue. It may begin after a minor skin break, injection, surgical wound, burn, childbirth injury or no obvious portal. Pain can be far greater than the visible skin changes, and early skin findings may look like cellulitis. Delay in surgical source control causes tissue necrosis, septic shock, organ failure, amputation and death. Emergency providers must escalate early—antibiotics support but never replace urgent exploration and debridement.

Learning objectives

Define necrotizing fasciitis and distinguish it from cellulitis, abscess and other soft-tissue infections.
Recognise risk factors, early disproportionate pain, systemic toxicity, skin changes and Fournier’s gangrene.
Perform ABCDE, sepsis and limb/perineal assessment, obtain cultures and communicate urgency.
Describe emergency fluids, broad-spectrum antibiotics, toxin suppression, surgery, ICU and wound care.
Plan nursing, infection-control, rehabilitation, prevention and patient/family education.

Definition and pathophysiology

Necrotizing fasciitis is infection and thrombosis of the superficial fascia, deep fascia and surrounding subcutaneous tissue. Bacteria release enzymes and toxins that destroy tissue, impair perfusion and spread along fascial planes. Infection may be polymicrobial (aerobic and anaerobic organisms) or monomicrobial, commonly involving group A Streptococcus, Staphylococcus aureus, Gram-negative organisms or anaerobes. Type I disease is often polymicrobial; type II is commonly group A streptococcal or staphylococcal.

As fascia becomes necrotic, analgesia-resistant pain, oedema, systemic inflammatory response, capillary leak and septic shock develop. Skin may initially appear relatively normal because the infection spreads beneath it. Later there may be bullae, dusky or purple skin, anaesthesia, crepitus, foul drainage and black necrosis.

Risk factors and portals of entry

Risk factor	Examples	Clinical implication
Skin break/trauma	Cut, puncture, insect bite, abscess, injection, burn, surgery or pressure injury.	Ask about even minor trauma and inspect all wounds.
Metabolic/vascular	Diabetes, peripheral vascular disease, obesity, renal failure or malnutrition.	May blunt inflammatory signs and impair healing.
Immune suppression	HIV, steroids, chemotherapy, cancer, sickle cell disease or advanced illness.	Low fever or normal white count does not exclude severe infection.
Perineal/abdominal source	Perianal abscess, childbirth injury, urogenital infection or Fournier’s gangrene.	Inspect perineum respectfully; urgent surgical/urological review.
Water/animal exposure	Contaminated water, fish injury, animal bite or soil contamination.	Include unusual organisms in specialist antibiotic planning.

Clinical features

Severe pain out of proportion to the visible lesion, pain beyond the erythematous margin or rapidly escalating analgesic requirement.
Rapidly spreading redness, swelling, warmth, tense skin and oedema; fever, tachycardia, tachypnoea, weakness or confusion.
Skin anaesthesia from nerve destruction, bullae, dusky/purple/grey or black patches, crepitus and foul or “dishwater” discharge.
Sepsis or shock: hypotension, delayed capillary refill, oliguria, altered mental state, rising lactate and organ dysfunction.
Fournier’s gangrene: severe genital/perineal pain or swelling, skin discoloration, crepitus, urinary difficulty or systemic toxicity.

Red flags: pain disproportionate to examination, rapid progression over hours, systemic toxicity, skin anaesthesia, bullae/necrosis, crepitus, severe tenderness beyond redness, hypotension, confusion, diabetes/immunosuppression or infection of the perineum. Call surgery now; do not wait for imaging or a high LRINEC score.

First contact and infection control

Use gloves, gown, eye/face protection and hand hygiene; cover draining wounds and isolate contaminated materials according to facility policy.
Place the patient in a resuscitation area, remove constricting clothing/jewellery and protect the limb or perineum from pressure.
Activate emergency surgery, anaesthesia, infectious-disease/medical and ICU teams. State “suspected necrotizing soft-tissue infection with possible sepsis.”
Keep nil by mouth for likely debridement; provide analgesia, antiemetic and reassurance without delaying surgery.
Mark the edge of erythema with time/date for trend, but do not let marking or imaging delay theatre.

ABCDE and sepsis assessment

A — Airway

Assess consciousness, vomiting, facial/neck infection and airway swelling. Prepare early airway support for sepsis, shock or anaesthetic transfer.

B — Breathing

Measure respiratory rate, SpO₂ and work of breathing; tachypnoea may indicate sepsis, acidosis or pneumonia.
Give oxygen for hypoxaemia/distress and prepare ventilation support if respiratory failure develops.

C — Circulation

Check pulse, BP, capillary refill, temperature, urine output, lactate and peripheral perfusion.
Insert two IV lines where possible, collect blood cultures/labs and start isotonic crystalloid for shock under sepsis protocol.
Activate blood/vasopressor/critical-care support when hypotension persists, especially with extensive debridement or bleeding.

D — Disability

Record AVPU/GCS and bedside glucose; confusion, agitation or drowsiness may indicate sepsis, hypoglycaemia or shock.
Assess pain, sensation and motor function of the affected limb; new numbness suggests advanced tissue injury.

E — Exposure

Expose and inspect the entire limb/body, perineum, surgical wounds and pressure areas while maintaining dignity and warmth.
Look for crepitus, bullae, anaesthesia, rapidly advancing margin, foul drainage and compartment/vascular compromise.

Focused history and examination

Area	Questions/findings	Why it matters
Time course	When did pain/swelling begin? How rapidly has it spread? Any pain beyond the visible redness?	Rapid progression and disproportionate pain are key early warnings.
Portal of entry	Cut, injection, insect bite, abscess, surgery, childbirth, perianal infection, burn or water/animal exposure?	Guides source control and antibiotic coverage.
Systemic symptoms	Fever/rigors, vomiting/diarrhoea, dizziness, weakness, confusion or reduced urine?	Assesses sepsis and organ dysfunction.
Risk/medicines	Diabetes, HIV, steroids, chemotherapy, kidney disease, anticoagulants or recent antibiotics?	Predicts progression, resistant organisms and bleeding risk.
Examination	Vital signs, sensation, pulses, motor power, skin colour, bullae, crepitus, drainage, perineal/anal/urethral involvement.	Documents severity and identifies limb/perineal emergency.

Differential diagnosis

Cellulitis or erysipelas: superficial infection, usually slower and without severe pain beyond visible changes.
Abscess: localised fluctuance; can coexist with or progress to necrotizing infection.
Severe diabetic foot infection, infected ulcer or osteomyelitis.
Compartment syndrome, deep-vein thrombosis, acute limb ischaemia, pyomyositis or traumatic haematoma.
Vasculitis, calciphylaxis, pyoderma gangrenosum, necrotic tumour or severe allergic reaction.
Do not use a normal white count, normal temperature, normal early X-ray or low LRINEC score to exclude necrotizing fasciitis.

Investigations

Blood cultures before antibiotics when this causes no delay, full blood count, electrolytes, urea/creatinine, glucose, CRP, lactate, blood gas, coagulation and CK.
Deep tissue/wound cultures are obtained during surgery; superficial swabs may not reflect the deep pathogen.
Plain radiograph may show gas but a normal film does not exclude disease. CT/MRI can define extent only if the patient is stable and imaging will not delay exploration.
Ultrasound may identify fluid or gas but cannot safely rule out fascial infection.
Assess renal function, tetanus status, pregnancy, HIV/diabetes and nutrition to guide treatment.

Immediate medical management

Source control: urgent surgical consultation and aggressive exploration/debridement. CDC states primary treatment is early surgery and removal of necrotic tissue, coupled with broad-spectrum IV antibiotics.
Antibiotics: start broad-spectrum parenteral therapy immediately according to the local antimicrobial guideline, covering Gram-positive, Gram-negative and anaerobic organisms, including MRSA where indicated.
Toxin suppression: clindamycin is commonly added for documented or strongly suspected group A streptococcal disease; IDSA recommends penicillin plus clindamycin for confirmed GAS necrotizing fasciitis.
Resuscitation: treat sepsis/shock with isotonic fluid, oxygen when indicated, vasopressors and organ support in ICU.
Tetanus/wound care: update tetanus prophylaxis and cover wounds with sterile dressings; do not close infected necrotic wounds.

Surgical management

Explore beyond the visible skin changes, follow fascial planes and remove all devitalised tissue until healthy bleeding tissue is reached.
Leave the wound open for drainage and planned reassessment; CDC notes re-inspection around 24 hours is commonly required to confirm adequate debridement.
Repeat debridement is often necessary; amputation may be life-saving when tissue cannot be preserved or infection is uncontrolled.
Fournier’s gangrene may require extensive perineal, genital, colorectal or urological source control and urinary/faecal diversion decisions.
After infection control, reconstruction may include negative-pressure therapy, grafts, flaps and rehabilitation.

Nursing and EMT interventions

Trend vital signs, pain, skin margin, neurovascular status, urine output, lactate, glucose, renal function and response to fluids/antibiotics.
Use strict aseptic technique, correct PPE, wound isolation and safe disposal; protect staff from drainage and sharps.
Administer antibiotics on time, check allergies/renal dosing and monitor for anaphylaxis, nephrotoxicity, diarrhoea and line complications.
Maintain warming, pressure relief, nutrition, glycaemic control and analgesia; coordinate repeated theatre trips.
Provide psychological support, explain staged surgery and involve family with consent; prepare for body-image, amputation and rehabilitation needs.

Complications

Septic shock, disseminated intravascular coagulation, acute kidney injury, respiratory failure and multi-organ failure.
Compartment syndrome, limb ischaemia, tissue loss, amputation and severe scarring.
Necrotizing myositis, toxic shock syndrome, bacteremia and recurrent infection.
Hypothermia, hypoglycaemia/hyperglycaemia, malnutrition, pressure injury and venous thromboembolism.
Post-traumatic stress, depression, grief, sexual/urinary dysfunction and long-term rehabilitation needs.

Prevention and patient education

Clean and cover wounds promptly, seek care for spreading redness or increasing pain and do not squeeze abscesses.
Control diabetes, stop smoking, maintain nutrition and inspect feet/skin daily when neuropathy or vascular disease is present.
Complete prescribed antibiotics and return urgently for severe pain, fever, rapidly spreading swelling, numbness, blisters or dark skin.
Use safe injection, surgical and childbirth wound practices; ensure tetanus vaccination and infection-control procedures.
After discharge, provide wound/rehabilitation appointments, mobility aids, mental-health support and clear return precautions.

Clinical scenarios

Scenario 1 — “Cellulitis” with disproportionate pain: A diabetic man has a small red shin area but severe escalating pain, fever, tachycardia and new numbness. Treat as suspected necrotizing fasciitis: sepsis ABCDE, IV access, cultures without delay, broad-spectrum antibiotics, analgesia, fluids and immediate surgical review. Do not wait for CT.

Scenario 2 — Fournier’s gangrene: A patient has perineal pain, swelling, fever, foul drainage and confusion. Protect privacy, assess shock, give IV antibiotics/fluids under protocol, involve urology/general surgery/ICU and prepare for urgent extensive debridement. Do not apply topical creams or discharge for outpatient review.

Scenario 3 — Reassessment after theatre: Twenty-four hours after first debridement, pain, fever and skin discoloration continue. Escalate for repeat exploration; persistent disease after one operation is common and requires further source control, not reassurance.

Common errors to avoid

Calling it simple cellulitis because the skin looks mild early or because the patient is afebrile.
Waiting for CT, MRI, culture results or a laboratory risk score before surgical consultation.
Using antibiotics alone or closing a necrotic/infected wound.
Failing to inspect the perineum, feet, pressure areas or surgical wounds.
Giving large fluids without monitoring lungs/urine, or missing renal impairment and diabetes.

FASCIA NOW: F — Fatal emergency; A — Assess pain out of proportion; S — Sepsis ABCDE; C — Call surgery/ICU; I — IV access and broad antibiotics; A — Avoid delay for imaging; N — Necrotic tissue debridement; O — Open wound/re-look; W — Wound, rehab and prevention.

Revision questions

Why can necrotizing fasciitis look mild during the early phase?
List six red flags and five risk factors.
Why do antibiotics not replace surgical debridement?
What empirical antimicrobial coverage is required, and why may clindamycin be added?
Outline the immediate care of suspected Fournier’s gangrene.
Why should a low LRINEC score or normal imaging not end the assessment?

Key takeaways

Pain out of proportion plus rapid progression is necrotizing fasciitis until proven otherwise. Resuscitate, start broad IV antibiotics, call surgery immediately, debride aggressively, repeat exploration when necessary and support the patient through sepsis, tissue loss and rehabilitation.

References for further study

CDC. Clinical Guidance for Type II Necrotizing Fasciitis.
Infectious Diseases Society of America. Skin and Soft-Tissue Infection Guidelines.
WHO Essential Medicines Committee. Antibiotics for necrotizing fasciitis.
NHS. Necrotising fasciitis — warning signs and emergency care.
Follow current Uganda Ministry of Health antimicrobial, sepsis, surgery and infection-control protocols.

Necrotizing Fasciitis: Recognition, Resuscitation and Emergency Management Read More »

Dysmenorrhoea: Recognition, Assessment and Emergency Management of Painful Periods

Why this topic matters: Dysmenorrhoea is menstrual pain caused by uterine contractions and prostaglandins. Primary dysmenorrhoea commonly begins in adolescence and improves within about 72 hours; secondary dysmenorrhoea results from conditions such as endometriosis, adenomyosis, fibroids, pelvic infection or an obstructive anomaly. Most episodes are managed with planned analgesia, but severe or atypical pain can signal ectopic pregnancy, ovarian torsion, pelvic infection, haemorrhage, appendicitis or another emergency. Students should relieve pain while investigating red flags and protecting dignity.

Learning objectives

Define primary and secondary dysmenorrhoea and explain prostaglandin-mediated pain.
Recognise typical symptoms, atypical features and emergency red flags.
Take a menstrual, pregnancy, sexual-health, bowel/bladder and medication history sensitively.
Provide safe analgesia, supportive care, assessment and referral for persistent or severe pain.
Plan adolescent-friendly education, prevention of recurrence and endometriosis/pelvic disease follow-up.

Definition and physiology

Dysmenorrhoea means painful menstruation. In primary dysmenorrhoea, increased endometrial prostaglandins cause strong uterine contractions, temporary ischaemia and cramping without an identifiable pelvic disease. Pain usually starts shortly before or at the beginning of menstruation, may radiate to the back or thighs, and often improves over 1–3 days.

Secondary dysmenorrhoea is menstrual pain caused by pelvic pathology. Endometriosis is a common cause, but adenomyosis, fibroids, pelvic inflammatory disease, ovarian cysts, cervical stenosis, obstructive Müllerian anomalies and intrauterine devices may contribute. Progressive or treatment-resistant pain deserves investigation rather than repeated reassurance.

Primary versus secondary dysmenorrhoea

Feature	Primary	Secondary
Onset	Often begins 6–12 months after menarche when ovulatory cycles develop.	May begin later, after years of painless periods, or progressively worsen.
Timing	Starts just before/at bleeding and lasts up to about 72 hours.	May start well before bleeding, persist after it or occur between periods.
Associated features	Nausea, diarrhoea, headache, fatigue, back/thigh pain.	Dyspareunia, infertility, heavy/irregular bleeding, discharge, bowel/bladder pain or abnormal examination.
Examination/tests	Usually normal; diagnosis is clinical when red flags are absent.	May show tenderness, mass or abnormal imaging; investigate the underlying cause.
Response	Often responds to NSAIDs and/or hormonal treatment.	Requires cause-directed treatment and gynaecology referral if persistent.

Symptoms

Cramping suprapubic pain, low-back ache or pain radiating to the inner thighs.
Nausea, vomiting, diarrhoea, bloating, headache, dizziness, fatigue and faintness.
Heavy bleeding, clots, school/work absence, sleep disruption and reduced activity.
Severe pain with fever, discharge, dyspareunia, painful defecation, dysuria or infertility suggests secondary disease.

Emergency red flags: positive/possible pregnancy, sudden one-sided pain, syncope, shock, severe vomiting/dehydration, fever, guarding/rebound, heavy unexplained bleeding, new pelvic mass, acute urinary retention, blood in stool/urine or pain that is dramatically different from usual.

First contact and compassionate assessment

Provide privacy and ask the patient to describe the pain in their own words. Do not dismiss severe menstrual pain as normal or exaggeration.
Assess ABCDE and vital signs before routine analgesia questions; identify shock, infection, pregnancy and acute abdomen.
Ask consent before sensitive sexual/reproductive questions or examination. Offer a chaperone and adolescent-friendly communication.
Give appropriate analgesia early while continuing assessment; pain relief does not prevent diagnosis when the patient is reassessed.
Explain the plan, likely causes, warning signs and follow-up. Use teach-back rather than assuming understanding.

ABCDE assessment

A — Airway

Assess vomiting, consciousness and aspiration risk; support the airway if severe pain, opioid treatment or collapse occurs.

B — Breathing

Measure rate and SpO₂; consider pulmonary embolism, anaemia, sepsis or anxiety when breathlessness is present.

C — Circulation

Check pulse, BP, capillary refill, bleeding, hydration and temperature. Insert IV access if shock, severe vomiting or significant bleeding.
Give isotonic fluid for dehydration under protocol and reassess after each bolus.

D — Disability

Record AVPU/GCS and glucose when faint, confused, profoundly weak or medicated.
Assess distress, anxiety, self-harm risk and impact on school/work without labelling symptoms as psychological.

E — Exposure

Assess abdomen, pallor, fever, vaginal bleeding, discharge, scars and mass with consent and dignity.

Focused history

Area	Questions	Purpose
Pain pattern	When did it begin? Before or after bleeding? How long, how severe, one/both sides, radiating, different from usual?	Distinguishes primary pattern from torsion, ectopic, endometriosis or acute abdomen.
Menstrual	Age at menarche, cycle, flow, clots, irregularity, last period and bleeding between periods.	Assesses primary/secondary causes, anaemia and pregnancy.
Pregnancy/sexual health	Pregnancy possibility, contraception, sexual activity, discharge, dyspareunia and STI risk.	Pregnancy and PID can be emergencies; ask privately and respectfully.
Bowel/bladder	Painful stool/urination, constipation/diarrhoea, rectal/urinary blood.	Suggests endometriosis, infection or urinary/GI pathology.
Treatment response	What was taken, dose/time, effect, allergies, ulcer/kidney disease, anticoagulants and hormonal medicines?	Prevents NSAID overdose and guides safe treatment.
Impact/safety	Missed school/work, sleep, mood, bullying, abuse or inability to access menstrual products?	Supports holistic care and safeguarding.

Differential diagnosis when pain is severe

Condition	Clues	Urgent action
Ectopic pregnancy	Pregnancy possibility, unilateral pain, bleeding, shoulder pain, syncope or shock.	Pregnancy test, IV access, resuscitation and emergency gynaecology.
Ovarian torsion/cyst rupture	Sudden unilateral pain with vomiting, mass or peritoneal signs.	Urgent ultrasound/gynaecology; do not delay for analgesia response.
PID/tubo-ovarian abscess	Fever, discharge, pelvic tenderness, dyspareunia or sepsis.	Pregnancy test, antibiotics and admission/referral if severe.
Endometriosis/adenomyosis	Progressive pain, dyspareunia, bowel/bladder symptoms, infertility or heavy bleeding.	Gynaecology assessment and ultrasound; ongoing management plan.
Appendicitis/urinary/GI disease	Focal right lower-quadrant pain, urinary symptoms, diarrhoea, obstruction or fever.	General surgical/renal assessment and targeted tests.

Investigations

Pregnancy test in every patient of reproductive potential with significant pelvic pain or bleeding.
Full blood count for heavy bleeding/anaemia, urinalysis, STI testing when indicated, CRP and renal function before prolonged NSAIDs.
Pelvic ultrasound for atypical, severe, persistent or secondary dysmenorrhoea; a normal scan does not exclude endometriosis.
Further MRI, laparoscopy or specialist tests depend on suspected endometriosis, adenomyosis, fibroids, congenital obstruction or other pathology.

Acute treatment of primary dysmenorrhoea

Offer a non-steroidal anti-inflammatory drug (NSAID) early—often at the start of pain or bleeding—if not pregnant and without renal disease, ulcer, significant asthma sensitivity, anticoagulation or allergy. Follow local product dosing.
Paracetamol/acetaminophen may be used when NSAIDs are contraindicated or as advised; avoid duplicate combination products.
Use heat to the lower abdomen/back, comfortable positioning, hydration, rest, gentle movement and antiemetics if needed.
For severe refractory pain, use monitored titrated opioid only after dangerous causes are assessed; reassess sedation, respiratory rate and constipation.
Give a written plan for the next cycle rather than waiting until pain is maximal, and arrange review if treatment fails.

Hormonal and cause-directed care

Combined hormonal contraception, progestogen therapy or a hormonal intrauterine system may reduce ovulation, prostaglandin exposure and bleeding; discuss contraindications, pregnancy goals and adherence.
Suspected endometriosis needs a planned gynaecology pathway; severe pain despite NSAIDs/hormones, bowel/bladder pain, infertility or abnormal examination warrants referral.
Treat PID, fibroids, adenomyosis, anaemia, congenital obstruction and other causes according to specialist guidance.
In adolescents, do not delay endometriosis evaluation when pain causes school absence or persists despite empiric treatment.

Nursing and EMT interventions

Use a pain score, functional assessment and menstrual diary; reassess after medicine, heat and fluids.
Monitor vital signs, bleeding, hydration, nausea, renal function and medicine adverse effects.
Protect privacy; use respectful menstrual language and ask about access to pads, water, toilets and safe changing facilities.
Teach safe NSAID timing, contraindications, maximum prescribed dose and signs of GI bleeding/allergy/renal injury.
Provide school/work documentation when needed and arrange follow-up rather than repeated emergency-only visits.

Prevention and education

Track two or more cycles: pain score, bleeding, bowel/bladder symptoms, medicines, missed activities and mood.
Take prescribed NSAID early, maintain hydration, use heat and continue gentle activity when safe.
Seek urgent care for collapse, positive pregnancy test, sudden one-sided pain, fever, heavy bleeding, persistent vomiting or pain unlike usual.
Address anaemia, nutrition, menstrual hygiene and psychosocial distress; normalise help-seeking without normalising disabling pain.
Review contraception and fertility goals during hormonal treatment and refer for persistent/secondary symptoms.

Clinical scenarios

Scenario 1 — Primary pattern: A 15-year-old has cramping beginning with each period, normal examination and no red flags. Provide privacy, validate the pain, offer an age-appropriate NSAID plan if safe, heat, school support and follow-up; reassess if pain persists despite treatment.

Scenario 2 — Secondary warning: A 23-year-old has progressively worsening pain, dyspareunia and painful defecation despite NSAIDs. Arrange pregnancy/STI assessment and gynaecology referral for possible endometriosis rather than repeatedly treating “normal cramps.”

Scenario 3 — Emergency mimic: A patient reports “period pain” but is pale, faint, vomiting and has unilateral abdominal tenderness. Perform ABCDE, pregnancy test, IV access, fluids/analgesia and urgent imaging/gynaecology review for ectopic pregnancy, torsion or haemorrhage.

Common errors to avoid

Dismissing disabling menstrual pain as normal or assuming adolescents cannot have endometriosis.
Failing to check pregnancy before treating severe pelvic pain.
Giving NSAIDs despite pregnancy, renal disease, ulcer, anticoagulation or allergy, or combining multiple NSAIDs.
Using opioids repeatedly without reassessment, respiratory monitoring and a diagnostic plan.
Missing torsion, ectopic pregnancy, PID, appendicitis, urinary disease or severe anaemia.

PERIOD SAFE: P — Pregnancy test/red flags; E — Evaluate ABCDE; R — Record cycle/pain pattern; I — Investigate secondary causes; O — Offer early safe analgesia; D — Discuss hormonal options; S — School/work impact; A — Anaemia/STI screen; F — Follow-up; E — Escalate atypical pain.

Revision questions

Define primary and secondary dysmenorrhoea.
Explain the role of prostaglandins and why NSAIDs help.
List six red flags requiring emergency assessment.
Why is a pregnancy test important before treating severe pelvic pain?
When should an adolescent with painful periods be referred for possible endometriosis?
Outline safe patient education for NSAID use.

Key takeaways

Period pain deserves treatment and investigation when it is severe or atypical. Relieve pain early, check pregnancy and red flags, identify secondary causes, use medicines safely and arrange follow-up when symptoms impair life or fail to improve.

References for further study

ACOG. Dysmenorrhea: Painful Periods.
NICE Clinical Knowledge Summaries. Dysmenorrhoea: assessment and management.
WHO. Menstrual health and menstrual pain resources.
RCOG. Endometriosis and chronic pelvic pain patient information.
Follow current Uganda Ministry of Health and local gynaecology protocols for analgesia, STI care, pregnancy assessment and referral.

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Uterine Rupture: Recognition, Resuscitation and Emergency Obstetric Management

Why this topic matters: Uterine rupture is a tear through the uterine muscle, usually during late pregnancy or labour. It can cause catastrophic maternal haemorrhage, fetal hypoxia, fetal expulsion into the abdomen, shock and death. A previous caesarean or uterine surgery increases risk, but rupture can occur in an unscarred uterus with obstructed labour, trauma or excessive uterotonic stimulation. Abnormal fetal heart rate is often the earliest sign. Treat suspected rupture as a category-1 obstetric emergency—call the team, resuscitate and expedite laparotomy without waiting for imaging.

Learning objectives

Define complete and incomplete rupture and explain how scar, obstruction and uterotonic stress weaken the uterus.
Identify risk factors and early maternal/fetal warning signs during labour and after birth.
Perform immediate maternal ABCDE, fetal assessment, haemorrhage response and safe transfer.
Describe definitive surgical, anaesthetic, neonatal, transfusion and post-operative care.
Plan prevention through VBAC counselling, labour monitoring, safe induction and emergency preparedness.

Definition and types

Complete uterine rupture is a full-thickness separation of the myometrium and serosa, allowing the fetus, placenta or both to enter the peritoneal cavity. Incomplete rupture/dehiscence involves separation of the muscle with an intact serosa and may be less dramatic, but it still requires specialist assessment. Rupture may occur at a previous lower-segment caesarean scar, classical scar, myomectomy site, cornual area or an unscarred uterus.

Major maternal danger comes from rapid intra-abdominal bleeding, uterine vessel injury, bladder/ureter damage and shock. Major fetal danger comes from abrupt loss of uteroplacental perfusion, cord compression, hypoxia, prematurity and trauma.

Risk factors

Risk group	Examples	Clinical implication
Previous uterine scar	Previous caesarean, especially classical/upper-segment incision; prior rupture; myomectomy entering the cavity; uterine reconstruction.	Review operative records and plan birth in a facility with immediate emergency surgery and blood.
Induction/augmentation	Oxytocin or prostaglandins, especially high dose, prolonged labour or poor monitoring.	Use a written protocol, careful titration and continuous maternal/fetal monitoring.
Obstructed/overdistended uterus	Cephalopelvic disproportion, malpresentation, macrosomia, multiple pregnancy, hydrocephalus or grand multiparity.	Recognise prolonged labour, bandl’s ring, arrest and rising maternal/fetal distress early.
Trauma/procedures	Abdominal trauma, difficult instrumental delivery, manual procedures or external manipulation.	Assess for bleeding, pain and fetal compromise after trauma.
Unscarred uterus	Rare spontaneous rupture, placenta percreta, congenital anomaly or severe obstructed labour.	Do not exclude rupture because there is no scar history.

Clinical warning signs

Fetal: sudden prolonged bradycardia, recurrent late decelerations, loss of variability or persistent abnormal CTG—the most common early warning.
Maternal pain: sudden severe abdominal pain, pain between contractions, shoulder-tip pain or new tenderness; epidural analgesia can blunt pain.
Labour change: cessation of contractions, change in abdominal contour, loss of fetal station, presenting part rising or inability to hear fetal heart where previously clear.
Bleeding/shock: vaginal bleeding may be small despite major internal haemorrhage; tachycardia, pallor, sweating, dizziness, hypotension, oliguria and collapse are late signs.
Urinary signs: haematuria or blood at catheter insertion may suggest bladder injury.

Suspect rupture immediately when a woman in labour with a uterine scar develops an abnormal fetal heart rate, sudden pain, haemorrhage, maternal shock, loss of station or cessation of contractions. Do not wait for all signs to appear.

First contact and emergency activation

Shout for obstetric, anaesthetic, theatre, neonatal and blood-bank help. State: “suspected uterine rupture with maternal/fetal compromise.”
Stop oxytocin, prostaglandin or other uterotonic infusion immediately; do not continue augmentation while assessing.
Position supine with left uterine displacement or left lateral tilt, maintain airway and give high-concentration oxygen for maternal hypoxaemia or severe distress.
Apply continuous fetal and maternal monitoring if this does not delay theatre; prepare for immediate transfer to the operating room.
Do not perform forceful vaginal examination, instrumental delivery or repeated attempts to push the fetus down.

Maternal ABCDE resuscitation

A — Airway

Assess consciousness, vomiting and aspiration risk; call anaesthesia early because rapid deterioration and general anaesthesia may be required.
Suction and protect the airway as trained; maintain left uterine displacement during resuscitation.

B — Breathing

Measure respiratory rate, SpO₂ and work of breathing. Give high-flow oxygen for hypoxaemia, shock or fetal compromise according to local protocol.
Prepare assisted ventilation if exhaustion, reduced consciousness or massive haemorrhage causes respiratory failure.

C — Circulation and haemorrhage

Insert two large-bore IV cannulas if possible. Take full blood count, group/crossmatch, coagulation, fibrinogen, electrolytes, renal function and blood gas/lactate.
Start warmed isotonic crystalloid only as a bridge; activate the major obstetric haemorrhage/massive transfusion protocol early.
Monitor pulse, BP, capillary refill, mental state, urine output and response. Insert a urinary catheter when safe and record hourly output.
Use blood products and calcium/viscoelastic guidance according to the facility protocol; involve anaesthesia/critical care for vasopressor support if shock persists.

D — Disability

Record AVPU/GCS and bedside glucose; confusion/collapse indicates severe shock, hypoxia or medication effect.
Provide reassurance and explain actions briefly; do not leave the woman alone.

E — Exposure

Assess abdominal contour, tenderness, vaginal bleeding, fetal station, urine and surgical scars while preserving warmth and dignity.
Do not delay theatre for a complete examination or imaging when clinical suspicion is high.

Fetal assessment and neonatal preparation

Use continuous fetal heart monitoring when feasible; a sudden persistent bradycardia or pathological CTG is an indication for immediate obstetric action.
Document the last reassuring fetal heart rate, time of deterioration, contractions, medication doses and decision-to-delivery times.
Call the neonatal resuscitation team; prepare warmer, airway equipment, ventilation, umbilical access supplies and blood/glucose monitoring.
Do not delay maternal life-saving surgery for a prolonged fetal assessment. Delivery is usually by emergency laparotomy/caesarean unless the fetus has already delivered and the surgical team directs otherwise.

Investigations—but never at the cost of delay

Bedside haemoglobin may underestimate acute blood loss; trend laboratory haemoglobin, lactate, coagulation and fibrinogen while resuscitating.
Ultrasound may show free fluid or absent fetal location but is not required to confirm rupture in a crashing patient.
Crossmatch sufficient blood and prepare platelets/plasma according to the haemorrhage protocol.
Review previous operative notes, gestational age, placenta location, induction agents, oxytocin dose and fetal/maternal monitoring.

Definitive emergency management

Proceed to immediate laparotomy and delivery under the obstetric/anaesthetic team. NICE classifies suspected uterine rupture as a category-1 indication because it threatens the woman or fetus.
At surgery, control haemorrhage, deliver the fetus, assess the tear, repair the uterus when safe and fertility-preserving, or perform hysterectomy when bleeding, tissue damage or future risk makes repair unsafe.
Inspect bladder, ureters, bowel and broad ligament; involve urology/general surgery when injured.
Administer broad-spectrum antibiotics according to the caesarean/obstetric infection protocol and continue haemorrhage management.
After surgery, transfer to high-dependency/ICU if shock, coagulopathy, organ injury, massive transfusion or ventilation is required.

Postoperative and postpartum care

Monitor airway, breathing, circulation, uterine/vaginal bleeding, wound, drains, urine output, temperature, pain, haemoglobin, coagulation and electrolytes.
Assess for renal injury, DIC, sepsis, ileus, bladder injury, wound infection and thromboembolism.
Provide lactation and newborn support, analgesia, antibiotics and thromboprophylaxis as prescribed.
Explain operative findings, repair/hysterectomy, transfusion and future pregnancy implications sensitively and with an interpreter when needed.
Offer psychological first-line support; uterine rupture, emergency surgery, neonatal compromise or hysterectomy can be traumatic.

Nursing and EMT responsibilities

Record times precisely: recognition, stopping oxytocin, call for help, IV access, blood samples, blood products, theatre arrival and delivery.
Use two-person checks for blood, uterotonics, anaesthetic drugs and emergency infusions; monitor transfusion reactions.
Maintain left uterine displacement during initial resuscitation, keep the woman warm and provide clear updates to her chosen support person.
Prepare theatre and neonatal equipment, confirm allergies/consent where possible and transfer with full monitoring and resuscitation equipment.
Use SBAR handover including scar history, gestation, fetal tracing, maternal vitals, estimated blood loss, fluids/blood and drugs given.

Prevention and risk reduction

Review previous uterine surgery and operative records during antenatal care; counsel about planned repeat caesarean versus VBAC in an appropriate facility.
Offer continuous fetal and maternal monitoring for planned VBAC and ensure immediate caesarean, anaesthesia, blood and neonatal capability.
Use induction/augmentation only with clear indication, safe doses, careful cervical/contractile assessment and continuous monitoring where required.
Recognise prolonged/obstructed labour, malpresentation, macrosomia and rising maternal/fetal distress early; do not delay referral from a lower-level facility.
Educate the woman and family to report persistent scar pain, bleeding, faintness, reduced fetal movement or sudden change in labour immediately.

Clinical scenarios

Scenario 1 — VBAC bradycardia: A woman attempting VBAC develops sudden fetal bradycardia, abdominal pain and cessation of contractions. Stop oxytocin, call obstetric/theatre/neonatal teams, left lateral tilt, oxygen if indicated, two IV lines, blood sampling/crossmatch and immediate category-1 laparotomy. Do not wait for ultrasound.

Scenario 2 — Silent rupture with epidural: A woman with an epidural has recurrent pathological CTG, maternal tachycardia and loss of fetal station but little pain. Treat the CTG and station change as possible rupture; epidural does not exclude it. Activate theatre and resuscitation immediately.

Scenario 3 — Postpartum collapse: After difficult labour, a woman becomes pale and hypotensive with abdominal distension and little vaginal bleeding. Suspect concealed intra-abdominal haemorrhage, activate major obstetric haemorrhage, start resuscitation and expedite surgical assessment.

Common errors to avoid

Waiting for maternal hypotension or visible vaginal bleeding; fetal heart abnormalities may occur first.
Continuing oxytocin/prostaglandin or delaying theatre for ultrasound, paperwork or a complete vaginal examination.
Assuming an epidural excludes rupture because pain is minimal.
Using large volumes of crystalloid without early blood-bank/massive-transfusion activation.
Failing to prepare neonatal resuscitation or to document decision-to-delivery times.

RUPTURE NOW: R — Recognise fetal bradycardia/pain/shock; U — Uterotonics off; P — Phone obstetric, anaesthetic, theatre, neonatal and blood teams; T — Tilt left/oxygen/ABCDE; U — Use two IVs and crossmatch; R — Resuscitate with blood pathway; E — Expedite laparotomy; N — Neonatal resuscitation; O — Observe post-op; W — Watch for trauma, sepsis and coagulopathy.

Revision questions

Define complete versus incomplete uterine rupture.
List five risk factors and explain how induction/augmentation increases risk.
What fetal heart-rate change is often the earliest sign?
Why can an epidural mask the presentation?
Outline the first five actions when rupture is suspected.
What are the maternal and neonatal priorities during transfer to theatre?

Key takeaways

Suspected uterine rupture is a category-1 obstetric emergency. Stop uterotonics, call the full team, resuscitate the mother, monitor the fetus, activate blood support and expedite laparotomy—do not wait for classic pain, visible bleeding or imaging.

References for further study

WHO. A Pocket Guide for Clinical Management of Obstetric and Neonatal Emergencies in Africa.
NICE. Caesarean birth (NG192) — suspected uterine rupture as a category-1 emergency.
RCOG. Birth after Previous Caesarean Birth (Green-top Guideline No. 45).
ACOG. First and Second Stage Labor Management and VBAC resources.
Follow current Uganda Ministry of Health emergency obstetric and neonatal care, haemorrhage, blood-transfusion and referral protocols.

Uterine Rupture: Recognition, Resuscitation and Emergency Obstetric Management Read More »

Communication Essentials for Emergency Medicine and Health-Care Practice

Learning objectives

Definition of communication

Why communication is important in health care

The communication process

Modes of communication

The principles of effective communication

The 7 Cs

Additional clinical principles

Communication in the emergency encounter

Soft skills for the EMT and health worker

Patient-centred communication

Language, culture, disability and health literacy

Barriers to communication

Confidentiality, privacy and professional boundaries

Consent and shared decisions

Team communication and closed-loop safety

Communication during handover

Communication in difficult situations

Written communication foundations

Communication quality checklist

Scenario-based application

Common errors to avoid

Personal communication improvement plan

Quick revision questions

Key takeaways

Further reading

Hyponatraemia and Hypernatraemia: Emergency Assessment, Neurological Risks and Safe Correction

Learning objectives

Sodium physiology and definitions

Hyponatraemia: causes by volume status

Hypernatraemia: causes by water balance

Clinical features and red flags

Hyponatraemia

Hypernatraemia

First contact and safety

ABCDE assessment

A — Airway

B — Breathing

C — Circulation

D — Disability

E — Exposure

Investigations

Severe symptomatic hyponatraemia

Cause-specific hyponatraemia treatment

Hypernatraemia management

Neurological complications of correction

Nursing interventions

Admission, escalation and monitoring

Scenario-based application

Prevention and education

Common errors to avoid

Documentation checklist

Quick revision questions

Key takeaways

Further reading

Hypokalaemia and Hyperkalaemia: Emergency Assessment, ECG Recognition and Treatment

Learning objectives

Potassium physiology

Definitions and severity

Causes of hypokalaemia

Causes of hyperkalaemia

Clinical features

Hypokalaemia

Hyperkalaemia

Immediate contact and safety

ABCDE assessment

A and B — Airway and breathing

C — Circulation

D and E — Disability and exposure

ECG patterns

Investigations

Emergency management of hyperkalaemia

1. Stabilise the myocardium

2. Shift potassium intracellularly

3. Remove potassium from the body

Emergency management of hypokalaemia

Medication and cause-specific management

Monitoring after treatment