Acute care

A life-threatening generalised hypersensitivity reaction with rapid-onset Airway/Breathing/Circulation compromise and usually skin changes. The single most important action is prompt IM adrenaline — delay kills.

Life-threatening organ dysfunction from a dysregulated response to infection; septic shock is sepsis with persisting hypotension needing vasopressors + raised lactate despite fluids. Early recognition and the Sepsis Six save lives.

A state of inadequate end-organ perfusion. The exam tests assigning the mechanism — hypovolaemic, cardiogenic, distributive (sepsis/anaphylaxis/neurogenic) or obstructive — because the mechanism dictates the treatment.

Absent cardiac output requiring CPR and the Advanced Life Support algorithm. The pivotal split is the rhythm: SHOCKABLE (VF/pulseless VT — defibrillate) vs NON-SHOCKABLE (PEA/asystole — no shock), with reversible causes (4 Hs & 4 Ts) sought throughout.

Rapid large-volume blood loss causing hypovolaemic shock, coagulopathy and risk of death. Managed by activating the major haemorrhage protocol, controlling the source, and giving blood + tranexamic acid early.

A spectrum from unstable angina through NSTEMI to STEMI, driven by coronary plaque rupture and thrombosis. The pivotal split is the ECG/troponin: STEMI needs immediate reperfusion; NSTEMI/UA are risk-stratified and managed medically ± angiography.

Acute left-heart failure causing fluid to flood the alveoli — severe breathlessness, hypoxia and pink frothy sputum. An emergency treated by sitting the patient up, oxygen, IV nitrates and diuretics, while seeking the precipitant (ACS, arrhythmia, fluid overload).

Obstruction of the pulmonary arteries by thrombus (usually from a DVT). Presentation ranges from pleuritic pain/breathlessness to massive PE with haemodynamic collapse. The Wells score directs whether to image or D-dimer first; massive PE may need thrombolysis.

Air trapped under increasing pressure in the pleural space shifts the mediastinum and obstructs venous return — obstructive shock. A clinical diagnosis and an immediate-decompression emergency: do NOT wait for a chest X-ray.

A potentially fatal asthma exacerbation. Severity is graded (moderate / acute severe / life-threatening) on objective signs — and the dangerous trap is the SILENT chest and a normalising CO2, which signal exhaustion, not improvement.

An acute worsening of COPD with increased breathlessness, cough and sputum. The exam point is CONTROLLED oxygen via a Venturi mask in CO2 retainers (target 88–92%) and non-invasive ventilation for persistent respiratory acidosis.

A medical emergency of insulin deficiency: hyperglycaemia, ketosis and metabolic acidosis. Defined by the triad of ketonaemia ≥3 (or ketonuria ++), glucose >11 (or known diabetes) and acidosis (bicarbonate <15 or pH <7.3). Treated with fluids then a fixed-rate insulin infusion.

A type 2 diabetes emergency of profound hyperglycaemia, hyperosmolality and severe dehydration WITHOUT significant ketoacidosis (residual insulin suppresses ketogenesis). Onset is slower than DKA; fluid replacement is the mainstay and insulin is used cautiously.

A blood glucose below 4 mmol/L — a common, rapidly reversible emergency, usually from insulin/sulfonylurea therapy. Treatment depends on conscious level and IV access: oral fast carbohydrate if able to swallow, IV glucose or IM glucagon if not.

A raised serum potassium that threatens fatal arrhythmia. Severity and ECG changes drive urgency: cardiac protection with calcium gluconate first, then insulin–dextrose (± salbutamol) to shift potassium intracellularly, then removal.

Acute, life-threatening adrenal insufficiency — shock that responds poorly to fluids, with hyponatraemia, hyperkalaemia and hypoglycaemia. Often precipitated by illness/surgery or sudden steroid withdrawal. Treat with IV hydrocortisone immediately, before confirmatory tests.

The two endocrine extremes: thyroid storm (life-threatening thyrotoxicosis — fever, tachyarrhythmia, agitation) and myxoedema coma (decompensated hypothyroidism — hypothermia, bradycardia, reduced consciousness). Both are precipitated by illness/surgery and are clinical emergencies.

A seizure lasting ≥5 minutes, or repeated seizures without recovery between them — a neurological emergency. Managed by a timed, stepwise protocol: benzodiazepine first, then a second-line antiepileptic, then anaesthesia, while excluding hypoglycaemia and other causes.

A rise in intracranial pressure (mass, bleed, oedema, hydrocephalus) that threatens cerebral perfusion and risks herniation ("coning"). Recognised by the clinical triad and pupil/conscious-level change; managed by treating the cause and temporising measures.

Sudden focal neurological deficit from cerebral ischaemia. The emergency task is to confirm it is ischaemic (not haemorrhagic) on imaging and reperfuse within the window — thrombolysis (≤4.5 h) and/or thrombectomy for large-vessel occlusion.

Infection of the meninges — a medical emergency. In the community a non-blanching rash (meningococcaemia) warrants immediate benzylpenicillin; in hospital, do not let an LP delay antibiotics. Empirical IV ceftriaxone (± amoxicillin for Listeria cover) is given fast.

The commonest significant overdose. Toxic NAPQI accumulates once glutathione is depleted, causing delayed hepatic necrosis. Treatment is N-acetylcysteine, with the timed nomogram (or staggered-overdose rules) deciding who is treated.

Opioid toxicity causing the classic triad of reduced consciousness, respiratory depression and PINPOINT pupils. Naloxone reverses it — but it is short-acting, so re-sedation must be anticipated, especially with long-acting opioids (methadone).

A dangerous overdose causing the anticholinergic toxidrome plus the two killers: cardiotoxicity (sodium-channel blockade → broad QRS, arrhythmia) and seizures. IV sodium bicarbonate is the key antidote for QRS widening/arrhythmia.

Aspirin toxicity stimulates the respiratory centre (early respiratory alkalosis) and uncouples oxidative phosphorylation (metabolic acidosis) — the classic mixed acid–base picture, with tinnitus, hyperventilation and sweating. Treated with urinary alkalinisation; haemodialysis if severe.

Colourless, odourless gas (faulty boilers, fires, generators) that binds haemoglobin with high affinity, causing tissue hypoxia despite a NORMAL SpO2 on pulse oximetry (which cannot distinguish carboxyhaemoglobin). Treated with high-flow 100% oxygen.

Bleeding proximal to the ligament of Treitz — haematemesis/melaena. Risk-stratified by the Glasgow-Blatchford score (pre-endoscopy) and Rockall (post-endoscopy); variceal and non-variceal bleeds diverge in management (terlipressin + antibiotics for varices).

Tissue injury from heat, chemicals or electricity. Acute care centres on airway (inhalation injury), fluid resuscitation by the Parkland formula using % total body surface area (Wallace rule of nines), and appropriate referral.

A tear in the aortic intima lets blood track into the media, splitting the wall. A time-critical emergency: Stanford type A (ascending aorta) is surgical; type B (descending) is usually medical. The classic picture is sudden TEARING chest pain radiating to the BACK with a pulse/blood-pressure differential between the arms.

Accumulation of pericardial fluid (or blood) under enough pressure to compress the heart and impair filling — obstructive shock. The classic Beck triad is hypotension, raised JVP and muffled heart sounds, with pulsus paradoxus. It needs urgent echo and pericardiocentesis; rapid bleeds (trauma, type A dissection) cause it with small volumes.

A drug-induced hyperserotonergic state causing the triad of neuromuscular excitation, autonomic instability and altered mental state. It is a prescribing complication, not an idiosyncratic reaction — it comes on within hours of starting, escalating or combining serotonergic drugs, and resolves when they stop.

Core temperature outside the range the body can compensate for. Heat stroke is core temperature above roughly 40 °C WITH central nervous system dysfunction, and is distinguished from heat exhaustion by that CNS involvement. Hypothermia is core temperature below 35 °C, graded mild (32–35), moderate (28–32) and severe (<28).

Progressive, potentially reversible dysfunction of two or more organ systems following an acute insult — sepsis most often, but also trauma, pancreatitis, burns, major surgery or prolonged shock. It is the common final pathway of critical illness rather than a disease in itself, and it is why the treatment is always "fix the insult early".