General Surgery
Final Professional MBBS — General Surgery. Explanation-first answers that teach the reasoning behind every fact, with classifications, comparison tables, drug doses, clinical pearls and key-point recaps from Bailey & Love and SRB's Manual.
THE CONCEPT — WHAT SHOCK ACTUALLY IS
Shock is a state of acute circulatory failure in which the delivery of oxygen to the tissues is inadequate to meet their metabolic needs. The single most important idea to grasp is that shock is about tissue perfusion, not blood pressure — a patient can be in established shock with a still-normal blood pressure. When cells are starved of oxygen they switch to anaerobic metabolism, producing lactic acid; if perfusion is not restored, this progresses to cell death, organ failure and, ultimately, death. Everything else follows from thinking about what determines oxygen delivery.
Oxygen delivery depends on cardiac output (heart rate × stroke volume) and the oxygen content of the blood. Stroke volume in turn depends on preload (the volume returning to the heart), contractility (the pump), and afterload (the vascular resistance). Shock arises whenever one of these fails — and that gives us a logical classification.
CLASSIFICATION — BY THE MECHANISM THAT FAILS
Type Mechanism Common causes Hypovolaemic (commonest) Loss of circulating volume → low preload Haemorrhage, dehydration, burns Cardiogenic Pump failure → low output despite adequate volume Myocardial infarction, arrhythmia Distributive Loss of vascular tone → vasodilatation, blood pools, maldistribution Septic, anaphylactic, neurogenic Obstructive Mechanical block to filling/output Cardiac tamponade, tension pneumothorax, massive PE PATHOPHYSIOLOGY & STAGES — WHY EARLY SHOCK HIDES
Understanding the stages explains the clinical signs. In the compensated stage, baroreceptors detect the falling pressure and trigger a sympathetic response: the heart speeds up (tachycardia) and the peripheral vessels constrict to divert blood to vital organs. This is why an early-shock patient is tachycardic with cool, clammy skin, a prolonged capillary refill and reduced urine output — yet a still-normal blood pressure. The body is holding the pressure up by squeezing. In the decompensated stage, these mechanisms are exhausted, so blood pressure finally falls, perfusion worsens and acidosis deepens. If this continues, the irreversible stage supervenes — widespread cell death and multi-organ failure that no longer respond to treatment.
💡CLINICAL PEARL: This is the most important clinical lesson in shock: hypotension is a LATE sign. By the time the blood pressure drops, compensation has already failed and a large volume has often been lost. Recognise shock early from the perfusion signs — tachycardia, cool peripheries, prolonged capillary refill, oliguria and a rising lactate — and act before the pressure falls.CLINICAL FEATURES
The typical picture is tachycardia, a weak thready pulse, cool/pale/mottled clammy skin, prolonged capillary refill (> 2 s), tachypnoea, oliguria and altered mental state (anxiety → confusion → drowsiness), with hypotension appearing late. One important exception is early distributive (septic or anaphylactic) shock, where widespread vasodilatation makes the patient warm, flushed and bounding ('warm shock') before they eventually become cold as it decompensates.
MANAGEMENT — RESTORE PERFUSION, TREAT THE CAUSE
Resuscitation follows the ABC approach. Secure the airway and give high-flow oxygen; insert two large-bore IV cannulae (wide and short cannulae allow the fastest flow); and attach full monitoring. Then two things happen in parallel — restore the circulation and identify/treat the cause:
- Hypovolaemic/distributive shock — rapid fluid resuscitation with isotonic crystalloid boluses, reassessing after each; give blood for haemorrhage.
- Cardiogenic shock — fluids are given cautiously (the failing pump is easily overloaded); inotropes support contractility.
- Distributive/refractory shock — vasopressors (noradrenaline first-line) restore vascular tone once volume is replaced.
- Obstructive shock — relieve the obstruction (needle/tube decompression of a tension pneumothorax, pericardiocentesis for tamponade).
- Treat the cause definitively — stop the bleeding, give antibiotics and achieve source control for sepsis, adrenaline for anaphylaxis.
Response is judged not by blood pressure alone but by improving perfusion: a falling heart rate, warming peripheries, urine output above 0.5 mL/kg/hour, restored mental state and a clearing lactate.
DISTINGUISHING THE TYPES AT THE BEDSIDE
Although the initial resuscitation is similar, reading the clinical pattern points to the type and therefore the definitive treatment. Hypovolaemic shock gives cold peripheries with an obvious source of loss (bleeding, vomiting, burns) and a low CVP. Cardiogenic shock also has cold peripheries but with signs of a full circulation — a raised CVP/JVP, basal crackles, a gallop — because the problem is the pump, not the volume. Distributive (septic/anaphylactic) shock is classically warm and vasodilated early with a low CVP. Obstructive shock shows a high CVP with specific signs — tracheal deviation and absent breath sounds (tension pneumothorax), or muffled heart sounds (tamponade).
COMPLICATIONS OF PROLONGED SHOCK
If perfusion is not restored quickly, sustained tissue hypoxia damages every organ: the kidneys develop acute tubular necrosis (acute kidney injury), the lungs develop acute respiratory distress syndrome (ARDS), the gut mucosal barrier breaks down (allowing bacterial translocation and worsening sepsis), the clotting system may tip into DIC, and ultimately multi-organ dysfunction syndrome (MODS) supervenes. This cascade is precisely why early recognition and rapid restoration of perfusion — before the compensated stage fails — saves lives.
🔑KEY POINTS TO REMEMBER- Shock = acute circulatory failure with inadequate tissue oxygen delivery; it is about perfusion, not blood pressure.
- Types (by mechanism): hypovolaemic (commonest), cardiogenic, distributive (septic/anaphylactic/neurogenic), obstructive.
- Compensated stage keeps BP normal by tachycardia + vasoconstriction → cool clammy skin, prolonged CRT, oliguria; hypotension is a LATE sign.
- ABC + high-flow O2 + two large-bore cannulae; restore volume (crystalloid/blood) + treat the cause; inotropes/vasopressors for cardiogenic/refractory.
- Judge response by perfusion — heart rate, urine output >0.5 mL/kg/h, mental state, lactate clearance.
📚SOURCES: Bailey & Love's Short Practice of Surgery; ATLS.START WITH THE COMPARTMENTS — IT EXPLAINS EVERYTHING
To prescribe fluids sensibly you must first know where water sits in the body, because this determines where any fluid you infuse will end up. Total body water is about 60% of body weight — roughly 42 litres in a 70 kg man. Of this, two-thirds is intracellular (ICF, ~28 L) and one-third is extracellular (ECF, ~14 L). The ECF is itself split, with three-quarters in the interstitium (~10.5 L) and only one-quarter in the plasma/intravascular space (~3.5 L). That last figure is the key: the intravascular compartment — the one that keeps the circulation going — is small, and different fluids reach it to very different degrees.
TYPES OF FLUID — AND WHERE EACH ONE GOES
This is the heart of the topic. Fluids are either crystalloids or colloids:
- Isotonic crystalloids (0.9% saline, Ringer lactate/Hartmann's) — distribute throughout the whole ECF. Since only about a quarter of the ECF is intravascular, only ~25% of what you infuse stays in the circulation — so you need roughly 3 times the volume of blood lost to refill the intravascular space. These are the fluids for resuscitation and replacement.
- 5% dextrose — the glucose is quickly metabolised, leaving free water that distributes across TOTAL body water. Almost none stays intravascular, so it is useless for resuscitation; it is used to provide free water for maintenance.
- Colloids (albumin, gelatins, starches) — contain large molecules that exert oncotic pressure and so stay in the intravascular space longer, expanding plasma volume with a smaller infused volume — but they are costlier and carry specific risks (allergy; starches are now largely avoided).
💡CLINICAL PEARL: This single principle answers the commonest viva question: you resuscitate a shocked patient with isotonic crystalloid (or blood), never with 5% dextrose — because dextrose spreads across all the body water and barely fills the circulation, whereas isotonic crystalloid at least keeps a useful fraction intravascular.THE THREE PURPOSES OF FLUID THERAPY
Every fluid prescription serves one of three distinct purposes, and muddling them causes errors:
Purpose What it does Typical fluid Maintenance Replaces normal ongoing losses (urine, insensible, stool) Dextrose-saline / balanced + K⁺ Resuscitation Rapidly restores circulating volume in shock Isotonic crystalloid boluses / blood Replacement Replaces abnormal losses (vomiting, NG aspirate, fistula, third-space) Match the composition of the fluid being lost MAINTENANCE REQUIREMENTS
A person at rest needs roughly 30–35 mL/kg/day of water, about 1–2 mmol/kg/day of sodium, and about 1 mmol/kg/day of potassium, plus some glucose to limit ketosis. In children the Holliday-Segar ('4-2-1') rule is used: 4 mL/kg/h for the first 10 kg, 2 mL/kg/h for the next 10 kg, and 1 mL/kg/h for each kg thereafter.
ASSESSING FLUID STATUS
Good prescribing depends on assessment. Look for dehydration (thirst, dry mucous membranes, reduced skin turgor, tachycardia, low JVP/CVP, oliguria, and in severe cases hypotension) or overload (raised JVP, oedema, basal crackles, gallop rhythm). Combine the history, a careful examination, the urine output, and where needed the CVP and biochemistry, then reassess frequently — fluid therapy is a continuous adjustment, not a single decision.
COMPOSITION OF COMMON IV FLUIDS
Fluid Nature Note 0.9% saline Isotonic crystalloid Na⁺/Cl⁻ 154 each; large volumes cause hyperchloraemic acidosis Ringer lactate (Hartmann's) Isotonic 'balanced' crystalloid More physiological electrolytes; lactate → bicarbonate 5% dextrose Isotonic in bag, provides free water Spreads across all body water — not for resuscitation Dextrose-saline Maintenance fluid Provides water + some sodium COMPLICATIONS OF FLUID THERAPY
Fluids are drugs and can harm. Under-resuscitation leaves the patient in shock with organ hypoperfusion. Over-resuscitation causes pulmonary and peripheral oedema, and tissue oedema that impairs wound and gut healing; large volumes of 0.9% saline additionally cause a hyperchloraemic metabolic acidosis (which is why balanced solutions like Hartmann's are often preferred). The remedy is careful assessment and frequent reassessment rather than a fixed prescription.
'THIRD-SPACE' LOSSES
In major surgery, sepsis or bowel obstruction, fluid is sequestered into a non-functional 'third space' (the inflamed gut wall, peritoneal cavity or interstitium). This fluid is lost from the circulation even though it remains in the body, causing hypovolaemia that must be replaced — and it later mobilises back into the circulation during recovery, a shift that must be anticipated to avoid overload.
🔑KEY POINTS TO REMEMBER- Total body water ≈ 60% of weight; 2/3 intracellular, 1/3 extracellular; of the ECF only ~1/4 (≈3.5 L) is intravascular.
- Isotonic crystalloid distributes through the ECF (only ~25% stays intravascular → need ~3× volume lost); 5% dextrose spreads across all body water (useless for resuscitation); colloids stay intravascular longer.
- Resuscitate with isotonic crystalloid/blood, NEVER 5% dextrose.
- Three purposes: maintenance (normal losses), resuscitation (restore volume), replacement (match abnormal losses).
- Maintenance ≈ 30–35 mL/kg/day water + Na 1–2 mmol/kg + K 1 mmol/kg (children: 4-2-1 rule); assess status clinically + urine output/CVP and reassess.
📚SOURCES: Bailey & Love's Short Practice of Surgery; SRB's Manual of Surgery.THE CONCEPT — WHY WE USE COMPONENTS
Modern practice almost never transfuses whole blood. Instead a single donation is separated into components, for two good reasons: one donation can then treat several different patients, and each patient receives only the part they actually need, avoiding the risks of the rest. Understanding what each component contains tells you exactly when to use it.
BLOOD COMPONENTS & THEIR USES
Component Contains Used for Packed red cells Red cells (plasma removed) Anaemia / restoring oxygen-carrying capacity (1 unit raises Hb ~1 g/dL) Fresh frozen plasma (FFP) All clotting factors Coagulopathy, warfarin reversal, DIC, massive transfusion Platelets Platelets Thrombocytopenia/platelet dysfunction with bleeding Cryoprecipitate Fibrinogen, factor VIII, vWF, XIII Low fibrinogen (DIC), specific factor replacement INDICATIONS — A RESTRICTIVE APPROACH
Because transfusion carries real risks, a restrictive threshold is used: red cells are generally given when haemoglobin falls below about 7 g/dL (a slightly higher trigger of ~8 g/dL in patients with cardiac disease), or in acute blood loss causing haemodynamic compromise. The decision rests on the patient's symptoms and physiology, not the number alone.
GROUPING & CROSS-MATCHING — THE SAFETY STEP
Every transfusion must be ABO and Rhesus (Rh) compatible. Group O negative is the universal donor (no A, B or Rh antigens to react against) and is used in dire emergencies; AB positive is the universal recipient. Before a routine transfusion, the patient's serum is cross-matched against the donor cells to detect any incompatibility. The commonest cause of a fatal reaction is a clerical error — the wrong unit given to the wrong patient — which is why bedside identity checks are non-negotiable.
TRANSFUSION REACTIONS — CLASSIFIED BY TIMING
It helps to think of reactions as immediate or delayed:
- Acute haemolytic reaction (the most dangerous) — usually ABO incompatibility from a clerical error. Recipient antibodies destroy the donor cells (intravascular haemolysis), causing fever, loin/back pain, hypotension, haemoglobinuria, DIC and acute renal failure. Stop the transfusion immediately.
- Febrile non-haemolytic reaction — recipient antibodies against donor white-cell antigens cause fever and chills; common and benign (reduced by leucodepletion).
- Allergic / urticarial — a reaction to donor plasma proteins; ranges from urticaria to anaphylaxis (classically in IgA-deficient recipients).
- TACO (transfusion-associated circulatory overload) — too much volume too fast → pulmonary oedema, especially in the elderly/cardiac patient.
- TRALI (transfusion-related acute lung injury) — donor antibodies trigger acute lung injury with hypoxia and pulmonary infiltrates.
- Delayed — delayed haemolytic reaction (days later), infection transmission (hepatitis B/C, HIV — now very rare with screening), and iron overload with repeated transfusion.
MANAGING A SUSPECTED REACTION
The immediate steps are the same whatever the cause: stop the transfusion, keep the IV line open with saline, re-check the patient's and unit's identity, and resuscitate (oxygen, fluids, support blood pressure). Then treat specifically — for a severe acute haemolytic reaction, maintain urine output and manage DIC and renal failure — and report the reaction, returning the unit and a fresh sample to the blood bank for investigation.
CHANGES IN STORED BLOOD (why fresh differs)
Understanding what happens to blood during storage explains several transfusion complications. Over its storage life, red cells progressively leak potassium (so stored blood is potassium-rich), 2,3-DPG falls (temporarily reducing oxygen offloading), platelets and clotting factors degrade (so stored blood does not correct coagulopathy), the blood becomes acidic and cold, and microaggregates form. These changes underlie the complications of massive transfusion.
AUTOLOGOUS TRANSFUSION
A patient can sometimes receive their own blood — collected pre-operatively (predeposit), salvaged and returned during surgery ('cell salvage'), or by haemodilution. This eliminates the risks of incompatibility and transmitted infection, which is its main appeal, though it is not suitable in cancer or infected fields.
PRINCIPLES OF SAFE TRANSFUSION
Because the deadliest reactions come from giving the wrong blood to the wrong patient (a clerical error), safety rests on rigorous checks: correct sample labelling at the bedside, formal group-and-cross-match, and a final bedside identity check of patient and unit by two people before starting. The transfusion is observed closely, especially in the first 15 minutes when severe reactions declare themselves.
🔑KEY POINTS TO REMEMBER- Component therapy: one donation treats several patients, each getting only what they need.
- Packed cells (anaemia, 1 unit ≈ +1 g/dL Hb), FFP (clotting factors), platelets (thrombocytopenia + bleeding), cryoprecipitate (fibrinogen).
- Restrictive trigger ≈ Hb <7 g/dL (<8 in cardiac disease); O-negative = universal donor, AB-positive = universal recipient; always cross-match.
- Acute haemolytic reaction (ABO incompatibility, usually clerical error) is the most dangerous — fever, loin pain, haemoglobinuria, DIC, renal failure; STOP the transfusion.
- Also: febrile non-haemolytic, allergic/anaphylaxis, TACO (overload), TRALI (lung injury), infection. First step for any reaction = stop transfusion, saline, recheck identity, resuscitate, report.
📚SOURCES: Bailey & Love's Short Practice of Surgery; SRB's Manual of Surgery.THE CONCEPT
Haemorrhage is the escape of blood from the circulation. It matters in surgery both as an emergency in its own right and as the commonest cause of hypovolaemic shock. Classifying a haemorrhage — by its source, its timing and the amount lost — is not academic: each classification directly guides how urgently and how you must act.
CLASSIFICATION BY SOURCE
- Arterial — bright red blood spurting in pulsatile jets (high pressure).
- Venous — darker blood welling out in a steady flow.
- Capillary — a generalised ooze from raw surfaces.
CLASSIFICATION BY TIMING — A HIGH-YIELD IDEA
The timing of bleeding after an injury or operation points to its cause, which is why this classification is so useful:
- Primary haemorrhage — occurs at the time of injury or surgery.
- Reactionary haemorrhage — occurs within 24 hours, typically as the blood pressure recovers after resuscitation and dislodges a clot, or a ligature slips.
- Secondary haemorrhage — occurs 7–14 days later, when infection erodes a vessel wall. Recognising this mechanism explains its delayed timing and its association with sepsis.
CLASSES OF HAEMORRHAGIC SHOCK (ATLS)
The ATLS system grades acute blood loss by physiology, and reading it carefully teaches an important point about compensation:
Class Blood loss Key findings Class I <15% (<750 mL) Minimal — slight tachycardia only Class II 15–30% (750–1500 mL) Tachycardia, narrowed pulse pressure, anxiety; BP still normal Class III 30–40% (1500–2000 mL) Tachycardia, hypotension, confusion, oliguria Class IV >40% (>2000 mL) Profound hypotension, lethargy, anuria — immediately life-threatening 💡CLINICAL PEARL: Notice how the pulse pressure narrows in Class II — before the systolic pressure falls. This is because the rising diastolic pressure (from vasoconstriction) is an early compensatory sign, whereas the systolic pressure only drops in Class III. It is the same lesson as in shock generally: frank hypotension is a late sign, and by Class III a patient has already lost a third of their blood volume.MANAGEMENT — 'STOP THE BLEEDING, RESTORE THE VOLUME'
The two priorities run together. Control the bleeding by direct pressure and elevation, a tourniquet for a limb, definitive surgery, or interventional radiology (embolisation). Simultaneously, restore circulating volume through two large-bore cannulae — initially with warmed isotonic crystalloid, then blood for significant loss. In major trauma, modern practice uses damage-control resuscitation: permissive hypotension (accepting a lower blood pressure until surgical control, so as not to 'pop the clot'), a massive transfusion protocol giving red cells, FFP and platelets in a balanced ~1:1:1 ratio, and tranexamic acid early. Throughout, one aims to avoid the 'lethal triad' of hypothermia, acidosis and coagulopathy, which reinforce one another and make bleeding impossible to stop.
METHODS OF ARRESTING HAEMORRHAGE
Bleeding is stopped by natural and artificial means. The body's own response is vessel retraction and constriction, then platelet plug and clot formation. Surgically, control is achieved by direct pressure and elevation first, then definitive measures — ligation or clipping of the vessel, diathermy (electrocautery), suture, topical haemostatic agents, a tourniquet for a limb, or angiographic embolisation by interventional radiology. Choosing the method depends on the vessel and the situation.
CONCEALED (INTERNAL) HAEMORRHAGE
Not all serious bleeding is visible. Concealed haemorrhage into the chest, abdomen, pelvis or around a long-bone fracture can rapidly cause shock with no external blood loss — so in a shocked trauma patient one must actively look for hidden bleeding (e.g. with FAST ultrasound of the abdomen). This is why the shocked patient with no obvious wound still needs a systematic search for the source.
ASSESSING BLOOD LOSS
Blood loss is estimated from the physiological response (the ATLS class — heart rate, pulse pressure, mental state and urine output), rather than from the visible blood alone, because young patients compensate so well that a large loss may be masked until sudden collapse.
REACTIONARY vs SECONDARY — THE MECHANISM MATTERS
It is worth dwelling on why the timing tells you the cause. Reactionary bleeding appears within hours because the event that caused it is mechanical — as the patient warms and the blood pressure is restored by resuscitation, a small vessel that had gone into spasm reopens, a clot is washed away, or a ligature slips. Secondary bleeding appears a week or two later because the cause is biological — infection in the wound gradually erodes the wall of a vessel until it gives way. So the same symptom (bleeding) at different times demands different thinking: re-explore and secure the vessel for reactionary bleeding; control infection and often ligate the vessel more proximally for secondary bleeding.
🔑KEY POINTS TO REMEMBER- Haemorrhage = escape of blood from the circulation; classify by source, timing and amount.
- By source: arterial (bright, spurting), venous (dark, steady), capillary (ooze).
- By timing: primary (at injury), reactionary (<24 h, clot dislodges/ligature slips), secondary (7–14 d, infection erodes vessel).
- ATLS classes I–IV by % loss; pulse pressure narrows in Class II before systolic falls in Class III — hypotension is late.
- Stop the bleeding (pressure/tourniquet/surgery/embolisation) + restore volume (crystalloid then blood); trauma → permissive hypotension, 1:1:1 massive transfusion, tranexamic acid, avoid the lethal triad.
📚SOURCES: Bailey & Love's Short Practice of Surgery; ATLS.THE CONCEPT — A DYSREGULATED RESPONSE
Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. The crucial word is dysregulated: the damage in sepsis is done not only by the microbe but by the body's own overwhelming inflammatory reaction to it. Septic shock is the most severe form — sepsis with profound circulatory and metabolic derangement, defined as persistent hypotension requiring vasopressors to maintain a mean arterial pressure ≥ 65 mmHg together with a raised lactate (> 2 mmol/L) despite adequate fluid resuscitation — and it carries a high mortality.
PATHOPHYSIOLOGY — WHY THE PATIENT IS 'WARM' THEN COLD
Infection triggers a massive release of inflammatory mediators that act on the circulation in several damaging ways at once: widespread vasodilatation (which drops the blood pressure and, early on, makes the patient warm and flushed), increased capillary permeability (fluid leaks out of the vessels, worsening the effective hypovolaemia), microvascular thrombosis (which can progress to DIC), and myocardial depression. The result is tissue hypoperfusion and cellular hypoxia even though the cardiac output may initially be high — this is why septic shock is the classic 'warm' (distributive) shock early, turning cold as it decompensates.
RECOGNITION
Sepsis should be suspected in any patient with a likely infection who develops fever or hypothermia, tachycardia, tachypnoea, altered mental state, and signs of poor perfusion (mottling, oliguria, a rising lactate). Bedside tools such as qSOFA (respiratory rate ≥ 22, altered mentation, systolic BP ≤ 100) flag patients at higher risk who need urgent assessment.
MANAGEMENT — THE FIRST HOUR ('SEPSIS SIX')
Sepsis is a time-critical emergency; the evidence is that acting within the first hour saves lives. A simple, memorable bundle is to take three and give three:
- Give — high-flow oxygen; IV broad-spectrum antibiotics (immediately after cultures); and IV fluid resuscitation (a crystalloid bolus, about 30 mL/kg).
- Take — blood cultures (before antibiotics if possible); serum lactate; and monitor urine output.
💡CLINICAL PEARL: For the surgeon, one principle towers above the rest: source control. Antibiotics and fluids cannot save a patient whose sepsis is being driven by undrained pus, dead tissue or an infected device — the collection must be drained, the dead tissue debrided, or the source removed. This is why 'find and control the source' sits at the centre of surgical sepsis management.ONGOING CARE
If hypotension persists despite adequate fluids, vasopressors (noradrenaline first-line) are started to restore vascular tone and maintain a mean arterial pressure ≥ 65 mmHg. The patient is managed in a high-dependency/intensive care setting with organ support as needed, guided by repeated assessment of perfusion and lactate clearance.
SIRS AND THE SPECTRUM
Historically, sepsis was framed around the Systemic Inflammatory Response Syndrome (SIRS) — two or more of: temperature > 38 or < 36 °C, heart rate > 90, respiratory rate > 20, and abnormal white-cell count. SIRS plus a source of infection defined sepsis. Current definitions focus instead on organ dysfunction (measured by the SOFA score) as the marker that separates dangerous sepsis from an uncomplicated infection, because it is organ dysfunction that predicts death.
ORGAN DYSFUNCTION IN SEPSIS
The dysregulated response and hypoperfusion damage organs in a recognisable pattern — acute kidney injury (oliguria), acute lung injury/ARDS (hypoxia), altered mental state, deranged clotting/DIC, and hepatic and cardiovascular dysfunction — which together constitute multi-organ dysfunction syndrome (MODS), the common final pathway and the reason mortality is so high.
PREVENTION IN SURGICAL PATIENTS
Much surgical sepsis is preventable: asepsis, appropriate antibiotic prophylaxis, prompt treatment and drainage of infections, removal of infected devices, and early recognition of the deteriorating patient all reduce its incidence and severity.
WHY EARLY ANTIBIOTICS AND SOURCE CONTROL SAVE LIVES
The evidence in sepsis is stark: every hour of delay in effective antibiotics increases mortality, because the dysregulated response feeds on the ongoing infection. But antibiotics act on the bacteria in the blood and tissues — they cannot penetrate a walled-off collection of pus or sterilise dead tissue. This is the surgical crux: a septic patient with an abscess, an anastomotic leak, dead bowel or an infected implant will not recover on antibiotics and fluids alone, however aggressive, until the source is physically controlled — drained, resected or removed. Recognising the surgical source early, and dealing with it, is often the decisive intervention.
💊KEY DRUG DOSES (viva)- Fluid resuscitation — crystalloid bolus ≈ 30 mL/kg, reassessing.
- Vasopressor — noradrenaline infusion, titrated to MAP ≥ 65 mmHg.
- Broad-spectrum antibiotics per local protocol, immediately after cultures.
🔑KEY POINTS TO REMEMBER- Sepsis = life-threatening organ dysfunction from a DYSREGULATED host response to infection; septic shock = sepsis + vasopressor-requiring hypotension + lactate >2 despite fluids.
- Mediator storm → vasodilatation (warm shock), capillary leak, microthrombi (DIC), myocardial depression → tissue hypoperfusion.
- Recognise: fever/hypothermia, tachycardia, tachypnoea, altered mentation, mottling, oliguria, high lactate (qSOFA).
- First hour 'Sepsis Six': give O2, IV antibiotics, IV fluids (30 mL/kg); take cultures, lactate, urine output.
- SOURCE CONTROL is the surgical key (drain pus/debride/remove device); noradrenaline for fluid-refractory hypotension, target MAP ≥65.
📚SOURCES: Bailey & Love's Short Practice of Surgery; Surviving Sepsis Campaign.THE FUNDAMENTAL DISTINCTION
Intravenous fluids fall into two families, governed by one physical principle — the size of the dissolved particles decides whether the fluid can cross the capillary wall, and therefore where it ends up and how long it stays in the circulation. Crystalloids contain small molecules (electrolytes ± glucose) that pass freely across the capillary membrane; colloids contain large molecules that are retained within the vessels, where they exert an oncotic pull. Recall the compartments: total body water is ~60% of weight, two-thirds intracellular and one-third extracellular, and of the extracellular fluid only about a quarter (~3.5 L) is intravascular.
CRYSTALLOIDS
Isotonic crystalloids (0.9% saline, Ringer lactate, Plasma-Lyte) distribute through the whole extracellular fluid, so only ~25% stays intravascular — needing ~3× the volume of blood lost to refill the circulation; these are the resuscitation/replacement fluids. Hypotonic fluids (0.45% saline, dextrose-saline) give more free water for maintenance, and hypertonic saline (3%) is reserved for raised intracranial pressure and symptomatic hyponatraemia. 5% dextrose is effectively free water — it spreads across all body water and is never used for resuscitation.
COLLOIDS
Colloids are natural (albumin, FFP) or synthetic (gelatins, dextrans, hydroxyethyl starch). Their large molecules hold water intravascularly, so they expand plasma volume with a smaller infused volume and last longer — but they are costly and carry specific risks (dextrans → anaphylaxis and platelet dysfunction; starches → kidney injury and coagulopathy, and are now largely withdrawn).
COMPOSITION OF COMMON FLUIDS
Fluid Na⁺ Cl⁻ Note Plasma (reference) 135–145 95–105 — 0.9% saline 154 154 high Cl⁻ → hyperchloraemic acidosis in large volumes Ringer lactate 131 111 balanced; contains K⁺, Ca²⁺, lactate 5% dextrose 0 0 free water only — not for resuscitation 💡CLINICAL PEARL: Large trials (e.g. SAFE) show no survival benefit of colloids over crystalloids in most resuscitation, and some colloids cause harm — so the cheaper, safer crystalloid is first-line, with balanced solutions preferred over large-volume normal saline to avoid hyperchloraemic acidosis. Titrate to endpoints of perfusion (urine output > 0.5 mL/kg/h, clearing lactate), not to a fixed volume.PRESCRIBING FLUIDS IN PRACTICE
The prescription depends on the purpose. For maintenance, an adult needs about 25–30 mL/kg/day of water with ~1 mmol/kg/day each of sodium and potassium plus some glucose; in children the '4-2-1' rule gives the hourly rate (4 mL/kg for the first 10 kg, 2 for the next 10 kg, 1 per kg thereafter). For resuscitation, isotonic crystalloid is given as rapid boluses (250–500 mL in adults, 10–20 mL/kg in children), reassessing after each. Specific settings have their own regimens — ~30 mL/kg in early septic shock, the Parkland formula in burns, and normal saline in diabetic ketoacidosis.
REPLACING SPECIFIC LOSSES
Abnormal losses should be replaced with a fluid resembling what is lost. Gastric losses (vomiting, nasogastric aspirate) are rich in hydrogen, chloride and potassium — so prolonged vomiting causes a hypochloraemic, hypokalaemic metabolic alkalosis, corrected with saline and added potassium. Small-bowel, biliary and pancreatic losses are rich in sodium and bicarbonate, and diarrhoea or a high-output stoma loses large volumes — all measured and matched rather than guessed.
ENDPOINTS & COMPLICATIONS
Fluids are drugs and harm in either direction. Under-resuscitation leaves organs hypoperfused; over-resuscitation causes pulmonary and peripheral oedema and impairs wound and gut healing, while excess normal saline adds a hyperchloraemic metabolic acidosis. Therapy is therefore titrated to objective endpoints of restored perfusion — a falling heart rate, warm peripheries, capillary refill under 2 seconds, urine output above 0.5 mL/kg/h and a clearing lactate — with frequent reassessment rather than a fixed prescription. A useful discipline is to prescribe every fluid by its Drug (which fluid), Dose, Duration and De-escalation, exactly as for any other drug.
🔑KEY POINTS TO REMEMBER- Molecule size decides distribution: crystalloids cross capillaries; colloids are held in vessels by oncotic pressure.
- Crystalloids: isotonic (resuscitation — only ~25% stays intravascular, need ~3× loss), hypotonic (maintenance), hypertonic (raised ICP); 5% dextrose = free water, never for resuscitation.
- Colloids: natural (albumin, FFP) / synthetic (gelatins, dextrans, HES — HES withdrawn: AKI/coagulopathy).
- Crystalloid first-line (no survival benefit of colloids); prefer balanced solutions to large-volume saline; titrate to perfusion.
📚SOURCES: Bailey & Love's Short Practice of Surgery; SAFE study.WHAT IT IS AND WHAT IT REFLECTS
Central venous pressure (CVP) is the pressure in the great veins/right atrium, measured through a central line with its tip at the SVC–right-atrium junction and zeroed at the phlebostatic axis. It represents the right atrial pressure and therefore the preload — the volume returning to the right heart — which is why it is used as a guide to volume status. Normal is about 3–8 mmHg (≈ 5–12 cmH₂O).
INTERPRETATION
- Low CVP → hypovolaemia (the tank is under-filled).
- High CVP → fluid overload, right heart failure, or an obstructive cause (cardiac tamponade, tension pneumothorax); also raised by mechanical ventilation with high PEEP.
It is most useful dynamically: a fluid challenge (a small bolus) applies the Frank-Starling principle — an under-filled heart takes the extra preload with little rise in CVP, whereas a full or failing heart shows a sustained rise, signalling that more fluid will only congest.
THE CVP WAVEFORM
The trace follows the cardiac cycle — the a wave (atrial contraction), c wave (tricuspid bulge during ventricular contraction) and v wave (atrial filling). Abnormalities are diagnostic: giant a waves (tricuspid stenosis/pulmonary hypertension), cannon a waves (complete heart block), absent a waves (atrial fibrillation), and giant v waves (tricuspid regurgitation).
USES & RISKS OF THE LINE
A central line is placed by the Seldinger technique under ultrasound (internal jugular, subclavian or femoral vein) not only to measure CVP but to give vasopressors, TPN and rapid fluids and for dialysis access. Insertion carries real risks — pneumothorax, arterial puncture, air embolism, arrhythmias, and later catheter-related bloodstream infection — so it is done aseptically and removed early.
THE FLUID CHALLENGE & FRANK-STARLING
CVP is measured with a transducer zeroed at the phlebostatic axis, but its real clinical use is the fluid challenge: a small bolus (e.g. 250 mL) is given and the CVP watched. This applies the Frank-Starling principle — on the steep part of the curve (an under-filled heart) the extra preload raises stroke volume and the CVP barely moves; on the flat part (a full or failing heart) the same bolus gives little extra output but a sustained rise in CVP, warning that more fluid will only congest.
ALTERNATIVES & ADJUNCTS
Because CVP is imperfect, it is increasingly supplemented by better tools: an arterial line gives beat-to-beat pressure and pulse-pressure variation; bedside echocardiography shows cardiac filling and function directly (and IVC collapsibility); and dedicated monitors (PiCCO, oesophageal Doppler, or a pulmonary-artery (Swan-Ganz) catheter) measure cardiac output. These have largely displaced reliance on CVP alone in critical care.
INDICATIONS FOR CENTRAL ACCESS & SOURCES OF ERROR
A central line is placed for monitoring (CVP and central venous oxygen saturation) and for therapy — giving drugs that damage peripheral veins (vasopressors, concentrated potassium, chemotherapy, TPN), rapid large-volume infusion, temporary dialysis or a pacing wire, and reliable access when peripheral veins fail. A CVP reading is only as good as its technique: common errors include an incorrectly set zero reference (it must sit at the phlebostatic axis), measuring during coughing or straining, a blocked or malpositioned catheter, and high intrathoracic pressure in a ventilated patient — another reason the trend is trusted over any single value.
⚠️DANGER / REMEMBER: A key caveat: a single CVP value poorly predicts whether a patient will respond to fluid, because it is confounded by ventilation, cardiac function and vascular tone. Modern practice leans on dynamic measures — pulse-pressure/stroke-volume variation, passive leg-raise, response to a bolus — and echocardiography, treating CVP as just one strand alongside blood pressure, heart rate, urine output and perfusion.🔑KEY POINTS TO REMEMBER- CVP = right-atrial/great-vein pressure via a central line; reflects preload. Normal ≈ 3–8 mmHg (zeroed at phlebostatic axis).
- Low → hypovolaemia; high → overload, right heart failure, obstruction (tamponade/tension pneumothorax); PEEP raises it.
- Waveform: a (atrial contraction), c (tricuspid bulge), v (atrial filling); use the fluid challenge (Frank-Starling).
- Line also used for vasopressors/TPN/dialysis; risks — pneumothorax, arterial puncture, air embolism, line sepsis.
- A single CVP poorly predicts fluid responsiveness — prefer dynamic measures + overall perfusion.
📚SOURCES: Bailey & Love's Short Practice of Surgery.THE PRINCIPLE OF COMPONENT THERAPY
Component therapy separates one donation into its parts so the patient receives only the component they need. This is standard for two reasons: one donation then treats several patients, and each patient avoids the antigens and volume of the components they do not require. The guiding rule is to ask what the patient is short of and replace exactly that.
COMPONENTS, CONTENT & DOSING
Component Contains Indication / dose Packed red cells Red cells Anaemia — 1 unit raises Hb ~1 g/dL Fresh frozen plasma All clotting factors Coagulopathy, DIC, warfarin reversal — ~15 mL/kg Platelets Platelets Thrombocytopenia + bleeding — 1 pool ~+30×10⁹/L Cryoprecipitate Fibrinogen, factor VIII, vWF, XIII Low fibrinogen (e.g. DIC) Thresholds illustrate the reasoning: red cells at Hb below ~7 g/dL (~8 in cardiac disease); platelets below 10×10⁹/L prophylactically, below 50 before surgery; cryoprecipitate when fibrinogen falls below ~1 g/L.
GROUPING & CROSS-MATCHING
Every transfusion must be ABO and Rh compatible. Group O negative is the universal red-cell donor (used in emergencies) and AB positive the universal recipient; the serum is cross-matched against donor cells beforehand. The deadliest reaction is an acute haemolytic reaction from a clerical error (wrong unit to wrong patient), so bedside identity checks are mandatory and the patient is observed closely in the first 15 minutes.
MODIFIED PRODUCTS & STORAGE
Components can be tailored: leucodepleted (reduces febrile reactions/CMV), irradiated (prevents transfusion-associated graft-versus-host disease in the immunocompromised), and washed (for severe allergy). Each has its own storage need that sets shelf life — red cells 2–6 °C, platelets room temperature with agitation (~5–7 days), FFP/cryoprecipitate frozen. Whole blood is now rarely used.
TRANSFUSION REACTIONS — AN OVERVIEW
Every prescriber must know the reactions components can provoke. The most feared is the acute haemolytic reaction from ABO incompatibility — almost always a clerical error — causing fever, loin pain, haemoglobinuria, DIC and renal failure, and demanding that the transfusion be stopped immediately. Others include the common but benign febrile non-haemolytic reaction, allergic/anaphylactic reactions, TACO (circulatory overload → pulmonary oedema) and TRALI (transfusion-related acute lung injury), plus delayed haemolysis and infection.
THE STORAGE LESION & AUTOLOGOUS TRANSFUSION
During storage, red cells progressively leak potassium, lose 2,3-DPG, and become acidic and cold — the 'storage lesion' that underlies the hyperkalaemia, hypothermia and acidosis of large transfusions. Where possible a patient may receive their own blood (predeposited or intra-operatively salvaged) — autologous transfusion — which eliminates incompatibility and infection risk, though it is unsuitable in cancer or infected fields.
EMERGENCY RELEASE OF BLOOD
When there is no time for full cross-matching, blood is issued in escalating order of safety as time allows: immediate emergency group O (O-negative for women of childbearing age) → type-specific ABO/Rh-matched blood (a few minutes) → fully cross-matched blood (~45 minutes). Rh-negative status is protected in girls and women of childbearing age to prevent future haemolytic disease of the newborn. Safe transfusion is a process — correct sample labelling, group-and-save, a final two-person bedside identity check, and close observation, especially in the first 15 minutes when severe reactions declare themselves.
🔑KEY POINTS TO REMEMBER- One donation → several patients; give only the needed component.
- Packed cells (anaemia, +1 g/dL/unit), FFP (all factors, ~15 mL/kg), platelets (thrombocytopenia+bleeding), cryoprecipitate (fibrinogen).
- Thresholds: Hb <7 (<8 cardiac); platelets <10 prophylaxis, <50 pre-surgery; cryo if fibrinogen <1 g/L.
- ABO/Rh compatible + cross-match; O-negative universal donor, AB-positive universal recipient; clerical error is the deadliest risk.
- Modified: leucodepleted/irradiated/washed; storage — red cells 2–6 °C, platelets room temp with agitation, FFP/cryo frozen.
📚SOURCES: Bailey & Love's Short Practice of Surgery; SRB's Manual of Surgery.THE PARADOX AT ITS HEART
Disseminated intravascular coagulation (DIC) is inappropriate activation of clotting throughout the circulation. This creates the defining paradox: the widespread clotting consumes platelets and clotting factors faster than they can be replaced, so the patient clots and bleeds at the same time — microthrombi block small vessels and damage organs, while the exhausted clotting system bleeds from every wound and puncture site. It is never primary — always a complication of a serious illness.
PATHOPHYSIOLOGY
The trigger is usually release of tissue factor (from damaged tissue, tumour, or activated monocytes in sepsis), which ignites the cascade, generating thrombin that lays down fibrin microthrombi and consumes platelets and factors. The body then activates fibrinolysis to break down this excess clot, releasing fibrin degradation products including D-dimer — which themselves further impair clotting.
CAUSES
Classic triggers by category: sepsis (especially Gram-negative), major trauma/burns, obstetric emergencies (abruption, amniotic fluid embolism, retained products), and malignancy (especially acute promyelocytic leukaemia).
CLINICAL & LABORATORY PICTURE
There is bleeding (oozing from wounds/cannulae/mucosa) with thrombosis and organ dysfunction. Every lab value follows from consumption: factors used up → prolonged PT and aPTT; platelets consumed → low count; fibrinogen consumed → low fibrinogen; clot broken down everywhere → raised D-dimer/FDPs; the film may show schistocytes. It exists on a spectrum — acute (decompensated) DIC presents with bleeding (sepsis, abruption), while chronic (compensated) DIC may present with thrombosis (malignancy).
MANAGEMENT
Two arms: treat the underlying cause (essential — DIC will not settle while sepsis, retained products or the tumour persist), and supportive replacement of what is consumed — FFP, platelets and cryoprecipitate — for the actively bleeding patient. Heparin has only a limited, selective role where thrombosis predominates.
DIFFERENTIAL DIAGNOSIS
Several conditions mimic DIC. In liver failure, clotting factors are not made (prolonged PT) but the platelet-consumption and D-dimer picture is less marked, and factor VIII (made outside the liver) is normal. The thrombotic microangiopathies (TTP and HUS) cause thrombocytopenia and red-cell fragmentation but with normal PT/aPTT and fibrinogen, because they are platelet/endothelial disorders, not activation of the whole cascade. This contrast — deranged versus normal clotting times — is the key discriminator.
DIC IN SPECIFIC SETTINGS
In acute promyelocytic leukaemia, leukaemic cells drive severe DIC, and all-trans retinoic acid (ATRA) plus chemotherapy helps control it. In obstetric DIC (abruption, amniotic fluid embolism, retained products), emptying the uterus — removing the source — is definitive. In each case the DIC settles only when its trigger is removed.
WHY IT SELF-PERPETUATES, & SUPPORT
Part of why DIC becomes self-sustaining is that the body's own brakes on clotting — antithrombin, protein C and protein S — are consumed alongside the clotting factors, so thrombin generation continues unchecked throughout the circulation. For the bleeding patient, replacement is targeted to the deficits — FFP for factors, cryoprecipitate when fibrinogen is low (below ~1 g/L), and platelets for significant thrombocytopenia with bleeding — followed with serial platelet counts, PT/aPTT, fibrinogen and D-dimer. These measures only buy time; the disorder resolves only when the trigger is treated.
🔑KEY POINTS TO REMEMBER- DIC = system-wide clotting that consumes platelets/factors → simultaneous thrombosis AND bleeding; always secondary.
- Mechanism: tissue factor → thrombin → microthrombi + consumption → reactive fibrinolysis (D-dimer/FDPs).
- Causes: sepsis, trauma/burns, obstetric emergencies, malignancy.
- Labs (consumption): prolonged PT/aPTT, low platelets, low fibrinogen, high D-dimer/FDPs, schistocytes; acute (bleeding) vs chronic (thrombosis).
- Treat the cause + support with FFP/platelets/cryoprecipitate.
📚SOURCES: Bailey & Love's Short Practice of Surgery.POTASSIUM PHYSIOLOGY — WHY THE LEVEL MATTERS
About 98% of the body's potassium is intracellular, and this steep gradient sets the resting membrane potential of excitable tissues. Hyperkalaemia (serum K⁺ > ~5.5 mmol/L) is dangerous because a high extracellular potassium partially depolarises cardiac cells, destabilising the myocardium and risking fatal arrhythmias or arrest — often with little warning. It is therefore treated on the level and the ECG, not on symptoms.
CAUSES — THREE MECHANISMS
- Reduced excretion — acute/chronic kidney disease (commonest), Addison's, drugs (ACE inhibitors, ARBs, potassium-sparing diuretics, NSAIDs).
- Transcellular shift out of cells — metabolic acidosis, insulin deficiency, and tissue breakdown (crush injury, burns, rhabdomyolysis, tumour lysis, haemolysis).
- Increased load — potassium supplements and stored-blood transfusion.
Before treating, exclude pseudohyperkalaemia — a falsely high result from potassium leaking out of cells in the sample tube (haemolysed/delayed sample) — suspected when the level is unexpectedly high in a well patient with a normal ECG.
CLINICAL & ECG
It is often silent until the arrhythmia, though muscle weakness may occur. The ECG evolves in order: tall 'tented' T waves → flattened P waves and PR prolongation → widening QRS → sine wave → VF/asystole.
MANAGEMENT — STABILISE, SHIFT, REMOVE
Three logical steps, used together in a severe case: stabilise the myocardium with IV calcium gluconate (protects the heart but does not lower potassium); shift potassium into cells temporarily with insulin plus dextrose (± nebulised salbutamol, and correcting acidosis); and remove it with potassium binders or, definitively, dialysis. Stop contributing drugs, treat the cause, and monitor the ECG and glucose.
HOW THE COMMON DRUGS CAUSE IT
ACE inhibitors and ARBs reduce aldosterone, the hormone that drives renal potassium excretion — so blocking it retains potassium. Potassium-sparing diuretics (spironolactone, amiloride) act on the distal tubule to retain potassium, and NSAIDs reduce renal blood flow and aldosterone. These are especially dangerous in combination or in renal impairment, and are the first drugs to review in a hyperkalaemic patient.
THE EMERGENCY ALGORITHM
Confirm the level + attach ECG/monitor (exclude pseudohyperkalaemia) → Calcium gluconate IV — protect the myocardium → Insulin-dextrose ± nebulised salbutamol — shift K⁺ into cells → Potassium binders / dialysis — remove K⁺ from the body → Stop culprit drugs, treat the cause, recheck K⁺ and glucose
CONTRAST WITH HYPOKALAEMIA & CHRONIC CARE
It helps to hold the two disorders side by side: hyperkalaemia gives tall tented T waves, a widening QRS and asystole, whereas hypokalaemia hyperpolarises cells and gives the opposite — flat T waves, ST depression, prominent U waves and tachyarrhythmias. Beyond the acute emergency, chronic hyperkalaemia (usually renal) is managed by dietary potassium restriction, stopping or adjusting offending drugs, treating acidosis, potassium binders, and dialysis for established renal failure. In surgical patients, cautious potassium prescribing and awareness of the load from stored blood prevent it.
💊KEY DRUG DOSES (viva)- Calcium gluconate 10% — 10 mL IV over 5–10 min (cardioprotection); repeat if ECG changes persist.
- Insulin-dextrose — ~10 units soluble insulin in 50 mL of 50% dextrose IV.
- Salbutamol 10–20 mg nebulised; dialysis for definitive removal.
🔑KEY POINTS TO REMEMBER- 98% of K⁺ is intracellular and sets the membrane potential — high K⁺ destabilises the myocardium → arrhythmia/arrest.
- Causes: reduced excretion (renal failure, drugs), transcellular shift (acidosis, tissue breakdown), increased load (supplements, stored blood).
- Exclude pseudohyperkalaemia (haemolysed sample) if the patient is well with a normal ECG.
- ECG: tented T → flat P/long PR → wide QRS → sine wave.
- Stabilise (calcium gluconate) → shift (insulin-dextrose/salbutamol) → remove (binders/dialysis).
📚SOURCES: Bailey & Love's Short Practice of Surgery.THE MECHANISM
Anaphylactic shock is a severe form of distributive shock from an immediate (type I) hypersensitivity reaction. Prior sensitisation produces IgE that coats mast cells; on re-exposure, the allergen cross-links this IgE and triggers explosive release of histamine and other mediators, causing at once vasodilatation (hypotension), increased capillary permeability (fluid leaks out of vessels) and bronchospasm with mucosal oedema (airway compromise). An 'anaphylactoid' (non-IgE) reaction gives an identical picture through direct mast-cell activation (e.g. contrast) without prior sensitisation — treatment is the same. Common triggers: drugs (antibiotics, muscle relaxants), latex, contrast, colloids, stings and foods.
CLINICAL FEATURES
Onset is rapid: flushing, urticaria and angioedema of the lips/face; stridor from laryngeal oedema and wheeze from bronchospasm with hypoxia; and hypotension/shock, often with a sense of impending doom. Severity ranges from skin-only to airway compromise and collapse — any respiratory or cardiovascular involvement mandates immediate adrenaline.
RECOGNITION & PITFALLS
The diagnosis is clinical — rapid airway/breathing/circulation problems, usually with skin changes, after a likely trigger. Do not confuse it with a simple vasovagal faint (bradycardia and pallor but no urticaria, wheeze or angioedema). In the anaesthetised, draped patient, unexplained hypotension, high airway pressures or a rash may be the only clues.
MANAGEMENT — ADRENALINE FIRST
The life-saving action is immediate intramuscular adrenaline, which reverses the whole pathology: via α-action it vasoconstricts (raising BP, reducing oedema) and via β-action it bronchodilates and stabilises mast cells. Then remove the trigger, give high-flow oxygen, lie the patient flat with legs raised, and give a rapid IV fluid bolus. Antihistamines and corticosteroids are second-line adjuncts, not substitutes. Observe for a biphasic reaction (recurrence hours later); send mast-cell tryptase, and on discharge provide an adrenaline auto-injector and allergy referral.
THE RESUSCITATION SEQUENCE
Recognise anaphylaxis + remove the trigger; call for help → IM adrenaline into the anterolateral thigh (repeat every 5 min) → Airway: high-flow oxygen; prepare for early intubation if laryngeal oedema → Positioning: lie flat, legs raised (sit up only if breathing is the priority) → Rapid IV crystalloid bolus for hypotension → Refractory case: IV adrenaline infusion + senior/ICU help → Adjuncts (antihistamine, hydrocortisone); observe for a biphasic reaction
REFRACTORY ANAPHYLAXIS
A minority do not respond to repeated IM adrenaline and fluids. These patients need an IV adrenaline infusion under continuous monitoring by an experienced clinician, further fluid, and additional agents; patients on beta-blockers may respond poorly to adrenaline and can benefit from glucagon. This is why help is called early and the patient managed in a resuscitation area.
THE MEDIATORS & SEVERITY GRADING
The clinical picture maps onto the released mediators: histamine causes vasodilatation, vascular leak and bronchospasm; leukotrienes and prostaglandins intensify bronchoconstriction and leak; and tryptase is a useful diagnostic marker measured during and after the episode. Severity is graded from mild (skin/mucosa only), through moderate (respiratory or cardiovascular involvement — dyspnoea, wheeze, presyncope), to severe (hypoxia, hypotension, collapse). Prevention matters as much as treatment — take an allergy history before any prescription or anaesthetic, label allergies clearly, and refer previous reactors to an allergy service.
💊KEY DRUG DOSES (viva)- Adrenaline (IM) — adult 0.5 mg (0.5 mL of 1:1000), anterolateral thigh; repeat every 5 min as needed.
- IV fluids — rapid crystalloid bolus for hypotension; high-flow oxygen; adjuncts (antihistamine, hydrocortisone).
🔑KEY POINTS TO REMEMBER- Distributive shock from type I (IgE) hypersensitivity → mediator release → vasodilatation + capillary leak + bronchospasm; anaphylactoid = non-IgE, same picture.
- Triggers: drugs (antibiotics, muscle relaxants), latex, contrast, colloids, stings, foods.
- Rapid urticaria/angioedema + stridor/wheeze + hypotension; distinguish from vasovagal faint.
- IM adrenaline first-line and life-saving (α → vasoconstriction, β → bronchodilation): 0.5 mg 1:1000, repeat q5min.
- Add O2, positioning, IV fluids; antihistamine/steroid adjuncts; observe for biphasic reaction; tryptase + auto-injector + allergy referral.
📚SOURCES: Bailey & Love's Short Practice of Surgery; resuscitation council guidelines.DEFINITION
Massive transfusion is replacement of the patient's entire blood volume within 24 hours (or > 10 units of red cells in 24 h, or > 4 units in an hour). It is life-saving in major haemorrhage — trauma, ruptured aneurysm, major surgery, obstetric bleeding — but rapidly infusing large volumes of stored blood creates predictable problems, and understanding why each arises is the key to preventing them.
COMPLICATIONS & THEIR MECHANISMS
- Hypothermia — stored blood is cold; rapid infusion cools the patient, which itself impairs the clotting cascade and platelets. → warm all blood/fluids.
- Dilutional coagulopathy — stored red cells have few platelets/clotting factors, so replacing losses with red cells alone dilutes the patient's own clotting components.
- Hypocalcaemia — the citrate anticoagulant binds ionised calcium; large volumes drop calcium enough to impair clotting and cardiac function. → monitor/replace calcium.
- Hyperkalaemia — potassium leaks from stored red cells, so stored blood is potassium-rich.
- Acidosis — stored blood is acidic, adding to the acidosis of shock.
THE LETHAL TRIAD & DAMAGE-CONTROL RESUSCITATION
Hypothermia, acidosis and coagulopathy reinforce one another as the feared 'lethal triad', making bleeding impossible to stop. Older practice gave red cells first and caught up with plasma/platelets later — reliably producing dilutional coagulopathy. Damage-control resuscitation reverses this: transfuse red cells, FFP and platelets together in a balanced (~1:1:1) ratio from the outset (reconstituting whole blood), apply permissive hypotension until surgical control, give tranexamic acid early (CRASH-2), keep the patient warm, and proceed to damage-control surgery. Above all, control the bleeding source — transfusion only buys time.
MONITORING
Monitor for the specific complications — temperature, ionised calcium, potassium, acid-base and clotting — increasingly guided by viscoelastic tests (TEG/ROTEM) that show in near-real-time which component is deficient, allowing targeted rather than blind replacement. Note that fibrinogen falls earliest in major haemorrhage and is replaced with cryoprecipitate/fibrinogen concentrate.
THE MASSIVE TRANSFUSION PROTOCOL & EVIDENCE
Because massive haemorrhage is chaotic, hospitals use a pre-agreed massive transfusion protocol (MTP) activated with a single call, so the blood bank releases pre-defined packs of red cells, FFP and platelets in fixed ratios without waiting for individual requests. Two trials underpin practice: CRASH-2 showed early tranexamic acid reduces mortality in traumatic haemorrhage, and PROPPR supported the ~1:1:1 ratio.
VISCOELASTIC TESTING (TEG/ROTEM)
Conventional clotting tests are slow. Viscoelastic tests (TEG/ROTEM) analyse whole-blood clot formation, strength and breakdown at the bedside in near-real-time, showing which component is deficient — factors, fibrinogen, platelets or excess fibrinolysis — and so allow targeted, goal-directed replacement rather than blind fixed-ratio transfusion.
CONTROL THE SOURCE, & THE ROLE OF FIBRINOGEN
Massive transfusion responds to massive haemorrhage — major trauma, ruptured aneurysm, upper GI or obstetric bleeding — and one principle sits above the transfusion itself: definitive control of the bleeding source by surgery or interventional radiology, because no volume of blood saves a patient who continues to bleed. Among the clotting components, fibrinogen falls earliest and most critically and strongly predicts continued bleeding, so modern protocols specifically replace it with cryoprecipitate or fibrinogen concentrate, often guided by viscoelastic testing — a frequently examined refinement of balanced resuscitation.
🔑KEY POINTS TO REMEMBER- Massive transfusion = ~1 blood volume in 24 h (or >10 units RBC).
- Complications: hypothermia, dilutional coagulopathy, hypocalcaemia (citrate binds Ca), hyperkalaemia, acidosis.
- Lethal triad = hypothermia + acidosis + coagulopathy, mutually reinforcing.
- Damage-control: balanced 1:1:1 from the start, permissive hypotension, early tranexamic acid, keep warm, control the source.
- Monitor temperature, ionised calcium, K⁺, acid-base, clotting (TEG/ROTEM); fibrinogen falls earliest.
📚SOURCES: Bailey & Love's Short Practice of Surgery; ATLS; CRASH-2.