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Induction — Surgery

143 diseases · 72 criteria · structured C/P · Inves · Mng

C/P — Clinical Presentation
Inves — Investigations
Mng — Management
Special — Pathognomonic / disease-unique

Homeostasis & the Stress Response

18 entries
1

Homeostasis (concept)

Special
  • Claude Bernard (mid-19th C) held the organism maintains constancy of the internal environment (milieu interieur) against external forces; Walter B. Cannon carried this further and coined the term homeostasis, tying survival to its maintenance
  • Failure of physiologic systems to buffer the organism against external forces -> organ + cellular dysfunction = clinically recognised as SHOCK (inadequate cellular perfusion + cell dysfunction)
2

Tissue injury - causes

Special
  • Trauma: mechanical (penetrating, blunt, blast), chemical, burns
  • Surgery: elective, emergency
  • Infection: primary cause of injury OR secondary complication of other injuries
  • Others: autoimmunity, ischaemia
  • Body injury = extensive local damage &/or systemic insult (infection, hypoperfusion, hypothermia, acid-base disturbance, pain); frequently both occur
  • BURNS -> highest level of hypermetabolism; INFECTION (as a secondary complication) -> highest level of protein catabolism
3

Stress response - controlling systems & signalling

Special
  • Three interacting controlling systems: CNS <-> endocrine <-> immune
  • Signalling between them: (1) afferent + efferent nervous signals, (2) hormonal adaptations, (3) systemic washout of locally produced substances (e.g. cytokines from microcirculation / immune cells)
  • The body's response has 3 arms: local inflammatory reaction, systemic physiological change, metabolic/biochemical alteration
4

Stress response - inflammatory component

Special
  • Recruitment + activation of neutrophils, monocytes, macrophages, lymphocytes
  • Production of reactive oxygen + nitrogen intermediates
  • Production of pro- and anti-inflammatory cytokines
  • Acute-phase changes of hepatic protein synthesis
  • Upregulation of procoagulant activity
  • Stimulates neural + endocrine responses
5

Stress response - neural & endocrine components

Special
  • Neural: augments cardiovascular function via the autonomic nervous system; activates hypophyseal-pituitary-adrenal axis (HPAA); neuro-immune interaction
  • Endocrine: promotes glycogenolysis; catabolises peripheral lean tissue + fat for gluconeogenesis; peripheral insulin resistance
  • Endocrine-immune interaction: innate + adaptive immunity are depressed in large part by the action of cortisol
6

Stress response - temperature control

C/P
  • Pulse + temperature changes (sympathetic fever)
Special
  • Core-temperature detection receptors lie in the preoptic area of the hypothalamus
  • Stimuli: hypothermia from prolonged visceral exposure in open surgery; inadequate substrate supply (starvation); loss of thermal insulating barrier (burns); inadequate hepatic blood flow (hypovolaemia); inadequate peripheral circulation, VC or VD (sepsis)
  • Effects - Pituitary: vasopressin, ACTH -> cortisol + aldosterone, TSH -> thyroxine; Suprarenal medulla: catecholamines
7

Stress response - water & salt retention

Special
  • Vasopressin (ADH) from posterior pituitary; secreted by cytokine stimulation of peripheral receptors (afferent neurological impulses), volume receptors in atria, osmoreceptors in anterior hypothalamus
  • Aldosterone from suprarenal cortex; secreted via CNS -> ACTH, the renin-angiotensin system, and directly from the suprarenal under the effect of electrolyte concentration
8

Stress response - coagulation changes

Special
  • Shift from hypercoagulability -> hypocoagulability
  • Hypercoagulability: increased platelet number + adhesiveness; increased fibrinogen
  • Hypocoagulability: increased fibrinolysins; decreased fibrinogen
9

Stress response - intermediary metabolism

Mng
  • Rx = nutrition + exercise (immunonutrition) to support healing/immune response and maintain protein / functional recovery
Special
  • Glycogen -> catabolised to increase glucose
  • Fats -> catabolised to increase glucose + fatty acids in the circulation (decreased in peripheral tissues)
  • Protein -> catabolised to glucose + amino acids for the immune response + phases of healing; protein catabolism -> loss of muscle mass -> impaired functional recovery
  • In severe sepsis + burns protein catabolism is even more marked and energy expenditure massively increases, fuelled by intense free-fatty-acid oxidation
10

Stress response to injury (general)

Special
  • yes - graded to the injury; metabolism + nitrogen excretion rise in direct proportion to degree of injury; changes CAN be modified by anticipating/preventing complications with ICU management (nutrition, prevention of secondary insults)
  • pituitary = 'the leader in the endocrine orchestra' (Sir Walter Langdon-Brown, 1931); sets the whole synchronous neuro-endocrine-inflammatory response in motion
  • mediators from injury travel up the spinal cord to the hypothalamus -> CRF -> pituitary secretes ACTH + GH; pancreas increases glucagon; thyroid + gonads only minor role; net = lipolysis, hepatic gluconeogenesis, protein breakdown, pyrexia, hypermetabolism
  • adrenal medulla -> adrenaline; hypothalamus -> noradrenaline (peripheral nerves) + CRH -> anterior pituitary -> ACTH -> cortisol/glucocorticoids; cytokines drive a parallel inflammatory arm
  • severity depends on SEVERITY + TYPE of injury; for speedy resolution avoid 'SO' = secondary insults (3 Is: Ischaemia, Infection, Inadequate oxygenation/hypoxia) plus ongoing trauma e.g. compartment syndrome
11

Stress response to surgery

Special
  • Counter-regulatory hormones (cortisol, glucagon, catecholamines) rise within minutes of beginning an operation
  • In uncomplicated surgery the endocrine response is short-lived (24-48 h) and only initiates protein catabolism; proinflammatory-cytokine-driven (TNF-alpha, IL-1, IL-6, IL-8) protein catabolism continues for up to 1 month after major surgery
  • Cytokine imbalance also contributes to anorexia, pyrexia, fatigue + fat catabolism
  • Typically starved for a period pre- and post-operatively; wound healing (+/- infection) needs catabolism of peripheral tissues, whose armamentarium is the hormonal changes in intermediary metabolism
12

Changing concepts of homeostasis in surgery

Mng
  • Elective surgery aim = REDUCE the need for a homeostatic response, by minimising the primary insult: minimal-access surgery + stress-free perioperative (enhanced-recovery) care
  • Emergency surgery aim = artificially AUGMENT the homeostatic response (resuscitation): close the open loop by timely intervention/source control (e.g. drainage of abdominal collections) + provide organ support (critical care) until homeostasis can return to normal
13

Cytokines post-elective surgery

Special
  • Elective surgery with an uneventful course induces only minor systemic inflammatory changes; the acute-phase response is proportional to surgery-related tissue trauma / severity of the procedure
  • Virtually all inflammatory mediators (cellular, cytokines, APPs) peak at postinjury day 1-2 and return to baseline by postinjury day 6-7
  • Persistent postoperative pain, stress, or a second insult will change this pattern
14

Elective surgery inflammatory response

Special
  • proportional to tissue trauma/severity; virtually all inflammatory mediators (cellular, cytokines, acute-phase proteins) PEAK at postinjury day 1-2 and return to baseline by day 6-7
  • persistent postoperative pain, stress, or a second insult changes the pattern
15

Infection modifying the stress response

Special
  • Directly: production of endotoxin
  • Indirectly, secondary to changes in: blood volume, oxygen concentration, substrate concentration, pain, and cytokines released from inflammatory cells
16

Vagal (cholinergic) anti-inflammatory reflex

Special
  • A neural circuit relays messages of localised injury to the brain via the nucleus tractus solitarius
  • Brain follows with hormone release (ACTH, glucocorticoids) into the systemic circulation + a sympathetic response
  • A real-time, site-specific vagal (parasympathetic/motor vagus) response releases acetylcholine at the injury site to curtail the TNF/IL-1-driven inflammatory cascade from activated immunocytes
17

Factors responsible for systemic responses

Special
  • major trauma (fractures, burns, head/abdo/chest injuries); infection/inflammation/sepsis; major operations (anaesthesia - esp head-down + pneumoperitoneum for laparoscopy, tissue trauma, blood/fluid loss); major CV events (MI, PE, stroke); haemorrhage + fluid infusion; hypoxia
  • EXCESS IV fluid - particularly 0.9% NaCl - causing interstitial oedema; also excess heat loss, pain, psychological stress, secondary effects on the blood, and starvation
18

Mediators of the stress metabolic response

Special
  • (1) from the site of injury (not directly related to lipolysis) and (2) neuroendocrine
  • directly stimulates suprarenal gland -> corticosteroids -> muscle proteolysis; stimulates local nerve endings -> CNS catecholamines (the 'forerunner' hormone) + HPA axis -> ACTH -> corticosteroids (the 'permissive' hormone)
  • TNF's effect on sepsis-induced muscle proteolysis is mediated primarily by glucocorticoids; IL-1 regulates muscle proteolysis by glucocorticoid-INDEPENDENT pathways

Ebb–Flow & Metabolic Response

9 entries
19

Ebb phase

C/P
  • Tachycardia, tachypnoea, vasoconstriction
  • Decreased cardiac output + oxygen consumption
  • Lower basal metabolic rate
  • Increased sodium + water retention
  • Shunting of blood from periphery to vital organs
Special
  • Early (<24 h) HYPOmetabolic phase (Cuthbertson); a coordinated response directed toward immediate survival of the organism
  • Starts with activation of local coagulation + innate immune factors; an insult of sufficient magnitude then triggers systemic inflammatory + endocrine responses
  • Driven by surges in plasma catecholamine, cortisol and aldosterone; features acute-phase protein (APP) production
20

Catabolic flow phase

C/P
  • Tachycardia, tachypnoea, peripheral oedema, fever
  • Hyperglycaemia, leukocytosis
  • Increased O2 consumption, increased CO2 production, increased minute ventilation
  • Elevated resting energy expenditure (REE), negative nitrogen balance
Special
  • HYPERmetabolic phase of explosive metabolic + immune activity, enhanced enzymatic function + tissue repair; follows the ebb phase if the person survives
  • Massive neuroendocrine flux: catecholamines, ADH, cortisol, insulin, glucagon, GH
  • Increased adrenergic stimulation raises the glucagon:insulin ratio (+ raised cortisol + cytokines) -> proteolysis + lipolysis to mobilise carbon sources for hepatic gluconeogenesis
  • Amino acids from skeletal-muscle + visceral protein catabolism -> taken up by liver (gluconeogenic substrates + hepatic protein synthesis) or used for enzyme synthesis + collagen deposition at the injury site
  • FFAs + ketone bodies from adipocyte lipolysis meet energy needs of other tissues; adipocyte glycerol = glucose precursor for the liver
  • Liver provides substrates via gluconeogenesis + ketone synthesis, detoxifies nitrogenous waste via urea, and elaborates APPs; renal blood flow + GFR increase to excrete nitrogenous by-products
  • Cytokines/adipokines disrupt capillary tight junctions -> vascular leak -> fluid + substrates flow toward the avascular injury area + interstitium
  • Catabolic process usually peaks at approximately 48-72 hours post-injury; if unchecked it depletes endogenous resources and becomes maladaptive
21

Anabolic flow phase

Special
  • Recovery/anabolic phase: surges in insulin, GH and insulin-like growth factor I (IGF-I) within 5-10 days of injury
  • Flux of protein, fluid + electrolytes back to the depleted intracellular space (particularly skeletal muscle)
  • Interstitial oedema is reabsorbed; excess fluid eliminated with a brisk diuresis
  • As the cellular space re-expands, ions (K+, Mg2+, PO4-) move from blood into the cells for electrochemical equilibrium
  • Intensity + duration of the flow phase roughly correlate to the extent + type of injury
22

Ebb-and-flow in chronic critical illness

Special
  • In chronically critically-ill patients the classic ebb-and-flow pattern is altered
  • Recurrent bouts of sepsis + other proinflammatory stimuli -> fluctuating metabolic demand that remains chronically elevated (does not return to normal)
23

Metabolic / Neuroendocrine Stress Response to Injury

Special
  • increase glucose, free fatty acids and amino acids in the circulation (energy + protein for healing); decrease them in the periphery → decrease muscle mass → decrease functional recovery
  • general response conserves fluid in the ebb phase + maximises cardiovascular function
  • stress hormone = catecholamines; permissive = glucocorticoids, glucagon, growth hormone; storage = insulin
  • catabolic hormones (catecholamines + glucocorticoids) drive proteolysis (muscle) + lipolysis (adipose) → hepatic gluconeogenesis + acute-phase protein synthesis
  • insulin inhibited by catecholamines; cortisol sensitises cells to catecholamines; GH & glucagon act as anti-insulins
  • changes in intermediary metabolism: glycogen catabolised → glucose; fats catabolised → glucose + FFA (↑ circulation, ↓ periphery); protein catabolised → glucose + amino acids for immune response & healing → muscle mass loss → impaired functional recovery
  • burns cause the highest level of hypermetabolism; secondary (complicating) infection causes the highest level of protein catabolism
  • peri-operative starvation + need for wound healing (± infection) requiring catabolism of peripheral tissues, driven by hormonal changes in intermediary metabolism
  • metabolic acidosis + increased sympathetic drive → ↑ respiratory rate & minute ventilation → ↑ CO2 excretion → compensatory respiratory alkalosis
24

Metabolic / catabolic response to injury

Special
  • catabolic -> muscle wasting; altered muscle protein breakdown + insulin resistance; hyperalimentation (overfeeding) does NOT aid recovery
  • (a) provide metabolic fuel sources; (b) provide amino acids for synthesis of acute-phase proteins and later wound healing in the anabolic phase
  • catecholamines inhibit insulin / promote glucagon / promote gluconeogenesis; corticosteroids induce peripheral insulin resistance in skeletal muscle + fat and promote proteolysis; glucagon releases glucose from glycogen + promotes lipolysis
  • cortisol can rise TENFOLD immediately after surgery and stay elevated days-weeks; GH + thyroid hormones inhibit insulin effects + promote catabolism; reduced insulin secretion blocks cellular glucose utilisation
  • 45% of body protein is structural (unavailable for metabolic interchange); the other 55% is circulating/intracellular; loss causes muscle weakness + immune deficiency
25

Simple starvation vs stressed starvation

Special
  • HYPOmetabolic; primary substrate = free fatty acids from lipolysis, with only small proteolysis to supply the ~300 kcal/day needed by glucose-dependent tissues; sustainable up to 90 days
  • a brief hypometabolic 'ebb' followed by a pronounced hypermetabolic 'flow'; hallmarks = catabolism, proteolysis and gluconeogenesis
26

Fuel for metabolism

Special
  • brain, liver and RBCs do NOT need insulin for glucose uptake; muscle + adipocytes have insulin-dependent transporters inhibited by fasting (spares glucose for essential cells)
  • glycogenolysis (liver + muscle glycogen) supplies the whole body ~8 h (up to 18 h) without carbohydrate intake
  • muscle glucose -> lactate during activity -> to liver -> pyruvate + glycogen (using ATP) -> glucose -> back to muscle
  • liver = primary gluconeogenesis centre (low-level in kidney + intestinal epithelia); hepatic gluconeogenesis inhibits glycolysis in liver but not other organs; substrates = lactate, pyruvate, alpha-ketoacids, glycerol, acetyl-CoA, plus BCAAs (leucine, isoleucine, valine), alanine + glutamine from muscle
  • liver converts fatty acids + amino acids to acetoacetate -> reduced to beta-hydroxybutyrate by beta-HB dehydrogenase using NADH; some acetoacetate -> acetone (fruity breath of DKA); ketones fuel brain, heart + skeletal muscle when glucose/FFAs absent -> protein-sparing
27

Stress-related hyperglycaemia (stress-induced diabetes)

C/P
  • raised blood glucose in critically ill / injured patients WITHOUT background diabetes
  • hyperglycaemia is a normal response to stress
  • increased risk of diabetic complications: sepsis, renal impairment, polyneuropathy
Mng
  • tight glucose control in surgical ICU = important quality-control measure (perioperative hyperglycaemia raises morbidity/mortality)
  • IV insulin infusion by sliding scale in ICU reduces morbidity and mortality
Special
  • insulin resistance from increased counter-regulatory hormones (temporary) plus increased glucose production
  • catecholamines + cortisol suppress pancreatic insulin release; glucagon stimulates glycogenolysis + gluconeogenesis
  • severity of the stress determines duration of the hyperglycaemic state ('stress-induced diabetes')

Cell Injury, Hypoxia & Inflammation

9 entries
28

Cell injury (reversible vs irreversible)

Special
  • biochemical and/or morphological changes when homeostasis is perturbed by adverse (noxious) influences
  • difference is mostly QUANTITATIVE; irreversibility recognised by changes in nuclear appearance + rupture of the cell membrane
  • stages: normal cell -> adaptation (stress) OR cell injury (injurious stimulus); mild/transient = reversible; severe/progressive = irreversible -> cell death (necrosis or apoptosis)
  • exogenous = physical (heat/cold), chemical (toxins/drugs), viruses + bacteria; endogenous = genetic defects, hormones, metabolites, cytokines
  • excessive/overly prolonged normal stimuli; inhibition of vital cell functions (oxidative phosphorylation or protein synthesis); deficiency of oxygen (MOST important cause); deficiency of essential nutrients/metabolites
  • cell injury can be induced in single cells / tissue culture; inflammation CANNOT - it needs vascularised multicellular tissue
29

Hypoxia / anoxia

Special
  • relative deficiency of oxygen = disproportion between O2 need and availability (reduced supply OR increased demand that cannot be met)
  • a complete block in the oxygen supply
  • inadequate supply (high altitude); airway (strangulation, drowning); in blood - inadequate oxygenation (lung disease), inadequate transport (anaemia), inadequate perfusion (heart failure/ischaemia); cellular (cyanide poisoning of cellular enzymes inhibiting respiration)
30

Ischaemic cell metabolism / lactic acidosis

Special
  • cells switch aerobic -> anaerobic when perfusion falls; anaerobic product = lactic acid -> systemic METABOLIC acidosis (NOT respiratory; product of aerobic respiration is CO2 cleared by lungs)
  • complement + neutrophils primed -> oxygen free radicals + cytokines -> epithelial/endothelial injury -> 'leaky' walls -> oedema -> worsens tissue hypoxia
  • glucose exhaustion -> Na/K pump failure -> lysosomal autodigestive enzyme release -> cell lysis -> intracellular K+ released into blood
31

Inflammation (mechanisms)

Special
  • vascular response, cellular response, humoral response (mediators of inflammation)
  • fever with sweating/chills (hypothalamic); tachycardia HR>90 (sympathetic); tachypnoea RR>20 (sympathetic + hyperventilation to combat metabolic acidosis); constitutional symptoms (anorexia, tiredness, weakness, drowsiness); labs = leucocytosis + elevated ESR
  • (1) accelerated marrow release of leukocytes mediated by IL-1 + TNF-alpha from inflammatory cells at the injury site; (2) if inflammation persists, macrophages + T lymphocytes produce colony-stimulating factors (CSFs) driving new marrow leukocyte formation
32

Inflammatory markers (ESR / CRP)

Special
  • rough measure of altered plasma-protein composition (rate RBCs separate from plasma), notably albumin + acute-phase reactants (CRP, alpha-1-antitrypsin, ceruloplasmin, fibrinogen, serum amyloid-associated protein)
  • CRP = sensitive biochemical assay of CRP concentration, used INSTEAD of the standard ESR
33

Cytokine / complement mediator cascade

Special
  • complement cascade; C3a + C5a = biologically active anaphylatoxins that induce proinflammatory cytokine release
  • TNF-alpha + IL-1 = key mediators; IL-6 induces T + B cells; IL-8 recruits/activates inflammatory cells at the injury site; IL-10 = key ANTI-inflammatory cytokine that inhibits the others
34

TNF-alpha

Special
  • released by macrophages + natural killer cells (NOT leukocytes); triggered when anaphylatoxins C3a/C5a are stimulated
  • vital early local response - promotes PMN adherence to endothelium, fibroblast prostaglandin production, neutrophil activation, and release of further cytokines from lymphocytes
  • deleterious when proinflammatory stimuli go unchecked -> cellular damage + multi-organ failure; anti-TNF-alpha antibody trials (NORASEPT, INTERSEPT) showed NO statistically significant outcome benefit
35

Catecholamines (physiology)

Special
  • circulating epinephrine mainly from the adrenal gland (a hormone); most circulating norepinephrine from synaptic nerve clefts (a neurotransmitter)
  • the enteric nervous system produces up to 37% of the body's norepinephrine and >50% of its dopamine
36

Cortisol in critical illness

Special
  • up to a SIXFOLD increase in free cortisol with critical illness; the rise is proportional to the degree of stress
  • induces an increase in alpha- and beta-adrenergic receptors, sensitises receptors to catecholamines, suppresses inflammation, and binds INTRACELLULAR steroid receptors

SIRS, Shock & MODS

6 entries
37

SIRS / Systemic Stress Response

Special
  • local inflammatory response — effectors: vascular endothelium, platelets/plasma factors, immune system; aims: localise injury, initiate repair, metabolic adaptation. General response — effectors: neural, endocrine, neuroendocrine; aims: maximise cardiovascular function, conserve fluid in ebb phase, metabolic adaptation, negative feedback on the local response
  • short-lived: oxygen free radicals, nitric oxide, endothelin, PAF, prostaglandins; longer-acting cytokines: TNF, IL-1, IL-2, IL-6, interferons
  • proinflammatory: IL-1α/β, IL-2, IL-6, IL-8, interferon, TNF, PAF; anti-inflammatory: IL-4, IL-10, IL-13, prostaglandin E2, TGF-β
  • recruitment/activation of neutrophils, monocytes, macrophages, lymphocytes; reactive oxygen & nitrogen intermediates; pro- & anti-inflammatory cytokines; acute-phase changes in hepatic protein synthesis; upregulation of procoagulant activity; stimulation of neural & endocrine responses
  • pulse & temperature changes (sympathetic fever); water & salt retention; changes in intermediary metabolism; biphasic coagulation change — hypercoagulability (↑ platelet number/adhesiveness, ↑ fibrinogen) then hypocoagulability (↑ fibrinolysins, ↓ fibrinogen)
  • ADH — via cytokine stimulation of peripheral receptors, atrial volume receptors, anterior-hypothalamic osmoreceptors; aldosterone — via CNS-ACTH, renin–angiotensin, and direct electrolyte effect on the suprarenal cortex
38

Neurogenic Shock

Special
  • HR normal or decreased, BP ↓, CVP ↓, SVR ↓, CO ↓ (loss of vasomotor tone)
39

Obstructive Shock

Mng
  • if non-sustained responder has high CVP → suspect obstructive/cardiogenic shock → manage before anaesthesia
  • intraoperative sudden BP drop with rising CVP → suspect rupture of an emphysematous bulla during ventilation
Special
  • HR ↑, BP ↓, CVP ↑, SVR ↑, CO ↓ (distinguished from bleeding by the raised CVP)
40

Hypoadrenal (Adrenal-Crisis) Shock

C/P
  • chronic asthmatic on corticosteroids → immunologically compromised, liable to hypoadrenal shock under surgical stress
Special
  • sudden drop of BP with low CVP that is unresponsive to volume resuscitation or vasopressors
41

MODS / MOF

Special
  • an initial insult primes the inflammatory response, then sequential events during the vulnerable period drive dysfunctional hyperinflammation; MOF can develop WITHOUT overt infection
  • MOF occurs in a bimodal distribution: early (within 3 days of the initial insult) and late (6-8 days after); blood transfusion is immunomodulatory + may be DETRIMENTAL; MOF incidence has actually INCREASED (improved initial survival of the critically ill)
  • SIRS is normally controlled by endogenous cytokine antagonists during repair; if the response to SIRS is inadequate, MODS follows ('just a step away from death')
42

Major burns (hypermetabolic response)

C/P
  • Case 9: third-degree 45% BSA burn = MOST intensive hypermetabolism
  • hypovolaemia from plasma loss + excessive evaporative water loss through denuded skin (more energy used)
Mng
  • operations may be needed: escharotomies or tangential scar excision (attending blood loss + anaesthetic insult)
Special
  • skin loss predisposes to secondary infection -> more catabolism
  • highest resting energy expenditure of the injury spectrum (~205% of normal REE)

Analgesia & Pain

23 entries
43

Physiology of pain (pain pathway)

Special
  • Transduction -> transmission -> perception -> modulation
  • Transduction: nociceptors detect the stimulus
  • A-delta fibres (fast) + C fibres (slow)
  • Perception in thalamus, limbic system + cortex
  • Modulation via descending inhibitory pathways + periaqueductal grey matter
44

Nociceptors

Special
  • Receptor sensitive to + responsible for transmitting pain stimuli
  • Injury, temperature, chemical + mechanical stimuli
  • Prostaglandins, potassium ions, histamine + bradykinin
45

Pain modulation (inhibitory vs increased excitability)

Special
  • Inhibitory vs increased excitability
  • Dorsal horn (gate control); spinal cord (GABA + glycine, descending brainstem projections); higher centres
  • Peripheral sensitisation; spinal cord central sensitisation; higher centres
46

Gate Control Theory

Special
  • Ab-fibre input activates the inhibitory interneuron -> closes the gate -> blocks the projection neuron
  • C-fibre input inhibits the interneuron -> opens the gate -> pain transmitted
47

Adverse physiological effects of pain

Special
  • Hyperventilation -> respiratory alkalosis
  • Increased O2 demand -> metabolic acidosis, MI
  • Thoracic pain impairs lung expansion / reduces compliance -> post-op chest infection
  • Increased neuroendocrine stress response; reduced immunological function
  • Delays post-op mobilisation; increases DVT risk; prolongs hospital stay
48

Biopsychosocial model of pain

Special
  • Pain experience shaped by biological, psychological + social contributors
49

Multimodal (balanced) analgesia

Special
  • Targeting multiple sites for safer analgesia; explicitly distinct from polypharmacy
  • Local anaesthetics, anticonvulsants, TCAs, opioids, anti-inflammatories
  • Anticonvulsants, opioids, tricyclic/SNRI antidepressants, alpha-2 agonist (clonidine), LA
  • Anticonvulsants, opioids, tricyclic/SNRI, alpha-2 agonist
50

Definitions: analgesia / anaesthesia / sedation

Special
  • Analgesia = relief from pain; anaesthesia = insensitivity to pain; sedation = reduction in level of consciousness
51

Paracetamol

Mng
  • 1 g every 6 hours in an adult
  • Routes: PO / PR / IV
Special
  • Inhibits prostaglandin synthesis in the CNS; analgesic + antipyretic
  • Low incidence - rash; liver impairment in overdose
52

NSAIDs

Special
  • Inhibit cyclo-oxygenase (COX) -> prevent prostaglandin synthesis
  • GI ulceration; renal impairment (reduced renal blood flow -> acute renal failure); asthma (10% NSAID-sensitive); bleeding (impaired platelet function)
  • Diclofenac (Voltaren/cataflam), ibuprofen (Brufen), aspirin, indometacin, naproxen, piroxicam
  • Celecoxib, rofecoxib, meloxicam
53

Strong opioids

Special
  • Mu-receptor agonists: morphine, pethidine, diamorphine, fentanyl, buprenorphine, hydromorphone, oxycodone
  • Analgesia, sedation, euphoria, cough suppression
  • Emesis/nausea-vomiting, respiratory depression, itching/pruritus, constipation, addiction, tolerance; occasionally urinary retention + CVS effects
54

Morphine (gold standard)

Mng
  • Under 70y: IM/SC ~10 mg, oral ~20 mg
  • Over 70y: IM/SC ~5 mg, oral ~10 mg
Special
  • Water-soluble; titrate according to pain; can be given 2-hourly; addiction rarely an issue
55

Weak opioids

Mng
  • Dihydrocodeine 30 mg 6-hourly (qds) PO
  • Codeine phosphate 60 mg 6-hourly PO/IM
  • Tramadol 50 mg 6-hourly PO/IV/IM
Special
  • Partially bind opioid receptors -> weak effect -> ceiling effect
56

Compound analgesics

Special
  • Combination of paracetamol + a weak opioid
  • Examples: co-proxamol, co-dydramol, co-codamol
57

Local anaesthetics

Special
  • Block sodium channels -> prevent Na flow in nerve impulse propagation
  • Lignocaine (lidocaine), bupivacaine (marcaine), levobupivacaine (chirocaine), ropivacaine
  • Topical (EMLA/Ametop - cannulation); infiltration (suturing); epidural/spinal (deliveries); peripheral nerve block (femoral/sciatic/ankle)
  • Tingling around mouth, tinnitus, confusion, agitation, metallic taste
  • Blurred vision, dysrhythmias, convulsions, arrest
58

Entonox

Special
  • 50% N2O + 50% O2; self-administered
  • Strong analgesic, weak anaesthetic; rapid onset + rapid elimination
  • Effective for short, sharp procedures; few side effects
59

Adjuvant / other analgesic drugs

Special
  • Amitriptyline (TCA), gabapentin (anticonvulsant), sumatriptan, diazepam, buscopan, baclofen, clonidine, ketamine
60

Patient-controlled analgesia (PCA)

Mng
  • Morphine 1 mg bolus with 5-min lockout
  • Patient must have a loading dose
  • No other opioids with PCA apart from MST/methadone; occasionally fentanyl if uncontrolled side effects or renal failure
  • Anti-syphon / anti-reflux giving set
Special
  • Post-op pain, trauma pain, pancreatitis, failed epidurals
  • Safe, time-saving, patient satisfaction, constant blood concentration, drug titration, patient control
  • Not suitable for all; IV access required; attached to a machine; equipment malfunction; opioid side effects
61

Regional analgesia / anaesthesia

Special
  • Continuous infusion - fentanyl + bupivacaine, or plain bupivacaine; +/- PCEA
  • Intrathecal LA + opioid (e.g. fentanyl, diamorphine)
  • One-shot or continuous; single or plexus block
62

PCEA (patient-controlled epidural analgesia)

Mng
  • Continuous infusion + patient-controlled bolus 5 ml with 15-min lockout
  • Patient education essential
Special
  • Improves pain relief, reduces side effects, lower cumulative doses, patient individualisation, improves satisfaction, reduces ward-nurse + pain-team/anaesthetist time
63

Spinals (intrathecal / subarachnoid analgesia)

Special
  • Spinal / intrathecal / subarachnoid - lower volume than epidural
  • Diamorphine good for pain relief; short-acting without a catheter
  • Nausea, urinary retention, sedation / respiratory depression
64

Nerve blocks

Special
  • Orthopaedic surgery, fractured ribs, gynae, hernias; part of multimodal approach; uses LA
  • Fewer side effects, better pain control, less GA, early discharge, better physiotherapy
  • Motor block, loss of sensation, risk of nerve damage, needs specialist + time, risk of drug toxicity
65

Non-pharmacological pain techniques

Special
  • Distraction, education, reassurance, information, imagery, relaxation, hypnosis
  • Counter-stimulation, exercise/mobilisation, immobilisation (traction), hot/cold application, massage, aromatherapy, TENS, acupuncture

Postoperative Complications

22 entries
66

Postoperative Atelectasis

C/P
  • Low-grade pyrexia, tachypnoea and tachycardia in the absence of infection
Mng
  • Good analgesia
  • Respiratory physiotherapy
  • Early mobilisation
Special
  • Atelectasis — collapse of basal alveoli within 48 hrs of surgery
  • Susceptible to (secondary) infection
67

Postoperative Pulmonary Edema

C/P
  • Distressed, rapid breathing
  • Crackles at lung bases
Mng
  • Oxygen
  • Diuretics
  • CPAP or IPPV
Special
  • Cardiac and non-cardiac (acute ARDS)
68

Pneumothorax

Inves
  • CXR
Mng
  • Tension pneumothorax → treat immediately with needle thoracocentesis
  • Intercostal drain
Special
  • Chest trauma, rib fractures, subclavian central venous line insertion, brachial plexus block, positive-pressure ventilation
69

Pulmonary Embolism / Postoperative VTE (DVT/PE)

Inves
  • DVT: venous doppler, venography
  • PE: V/Q scan, contrast CT pulmonary angiography
Mng
  • Prophylaxis for all at-risk: elastic stockings, intra-op foot/calf compression, post-op mobilisation, anticoagulation, spinal/epidural anaesthesia, laparoscopic surgery
  • Treatment: heparinisation, long-term anticoagulation, caval umbrella, embolectomy
Special
  • Obesity, pre-op immobility, smoking, long duration of surgery, previous DVT/PE, pelvic/hip surgery, hypercoagulability (thrombophilia), malignancy, OCP
  • PE: important cause of in-hospital death; V/Q mismatch; all at-risk should receive prophylaxis
70

Fat Embolism

Mng
  • Early fixation of fractures may prevent this complication
Special
  • Follows major orthopaedic injury to long bones
71

Postoperative Airway Obstruction

C/P
  • Drowsy patient lying supine
  • Vocal cord spasm
  • Bronchospasm in asthmatics
  • Airway bleeding
Mng
  • Humidified O2
  • Nebulized adrenaline
  • IV steroids
  • Nebulized beta agonists (Ventolin) + anticholinergics (Atrovent)
Special
  • Common with obstructive sleep apnoea (OSA)
72

Perioperative / Postoperative Myocardial Infarction

C/P
  • Often silent — classic signs masked by post-op analgesia
Inves
  • Compare ECG changes
  • Cardiac troponins
Mng
  • Prevention of hypotension, arrhythmias and heart failure
  • Pain control
  • Beta blockers, alpha agonist, GTN and antiplatelets
  • Seek senior cardiology advice
Special
  • Poor
73

Postoperative Arrhythmias

Special
  • Hypoxia/hypercapnia, K imbalance, acid-base disturbance, pain, tachycardia, infection, sympathetic stimulation, hypothermia, drugs, pyrexia
  • Underlying disease: IHD, valvular disease, cardiomyopathy, HTN, hyperthyroidism, diabetes, conduction abnormalities, PVD, raised ICP
74

Postoperative Hypertension

C/P
  • Systolic BP >140 mmHg / diastolic BP >90 mmHg
Special
  • Blood pressure changes
  • Pain, anxiety, full bladder; hypercapnia/hypoxia (OSA); sympathetic activation; raised ICP
  • Causes cardiac, cerebral and renal morbidity
75

Postoperative Hypotension

C/P
  • Sustained systolic BP <90 mmHg or MAP <60 mmHg
Mng
  • Hypoxia & hypovolaemia are life-threatening — require urgent reversal
Special
  • Heart, brain, kidney and liver are vulnerable
  • Sepsis, anaphylaxis, heart failure, dysrhythmias, epidural analgesia, drug toxicity, acid-base abnormalities
  • Metabolic acidosis causes V.Tach & hypotension due to decreased epinephrine
76

Postoperative Stroke

C/P
  • Suspect if delayed post-op arousal or loss of function (exclude metabolic derangement + drugs)
Special
  • Embolic or haemorrhagic
  • Carotid bruits, Hx of stroke/TIA, MI, thrombophilia, cardiac surgery, atrial fibrillation; risk rises with vascular/cardiac surgery from arterial manipulation
  • 4%
77

Postoperative Convulsions

Mng
  • O2
  • Anticonvulsant (benzodiazepine)
  • Correct underlying disorder
  • Thiamine (esp. alcoholics) + glucose
  • ? Surgical re-exploration
Special
  • Omission of anticonvulsant therapy; hypoxia, sodium abnormality, hypoglycaemia, alcohol withdrawal; local anaesthetic toxicity
  • Surgical triggers: carotid endarterectomy, cardiac surgery, neurosurgery
78

Peripheral Nerve Injury (positioning)

Mng
  • Prevent by meticulous positioning + cushioning pressure points
Special
  • Needle trauma, stretching or compression of a nerve
  • Patient factors: diabetics, thin, alcoholics; surgery duration >6 hrs and positioning
  • Arm abduction >90° ; common peroneal nerve (lateral position); ulnar nerve at elbow
79

Complications of Spinal & Epidural Anaesthesia

C/P
  • Post-dural-puncture headache (esp. 2nd day) from CSF leakage
  • Visual: blurred / double vision
  • Auditory: tinnitus, buzzing, popping
  • Hypothermia
  • Hypotension
Special
  • Permanent neurological deficit from direct trauma or haematoma (anticoagulated patients)
  • Infection of CSF or epidural space (exogenous or endogenous) → antibiotics + urgent neurological intervention
80

Postoperative Nausea & Vomiting (PONV)

Special
  • Younger females, intra-abdominal surgery, prior PONV history, opioid analgesics (incidence 5-30%)
  • Analgesia-related: respiratory depression, hypotension, urine retention, opioid pruritus
  • Minor: sore throat, dental damage, pressure area & eye problems, cannula site problems
  • Major/catastrophic (rare): anaphylaxis, aspiration pneumonitis, awareness (leads to PTSD), malignant hyperpyrexia
81

Postoperative Bleeding

Inves
  • Clotting screen for coagulopathy
  • Hb/Hct/x-match to judge transfusion need
  • Assess loss from drains for ongoing bleeding
Mng
  • Surgical exploration — sooner rather than later
  • Antifibrinolytic drugs help
Special
  • Distinguish surgical bleeding from a bleeding diathesis (tendency to bleed)
  • Hypothermia and hypertension worsen the blood loss
  • Platelet dysfunction and hyperfibrinolysis contribute
82

Thyroidectomy Complications (post-op airway obstruction)

C/P
  • Stridor
  • Difficulty breathing
  • Recognised usually within first 12 hrs post-op
Mng
  • Airway emergency: sit upright, give oxygen
  • Examine neck, wound site & drain; ? re-open wound on ward
  • Call anaesthetist & surgeon immediately
  • Re-intubation & re-exploration of the neck
Special
  • Haematoma & compression from post-op haemorrhage (first 24 hrs); tracheomalacia; hypocalcaemia & tetany from parathyroid removal (after 24 hrs, laryngeal dysfunction)
83

Postoperative Fever

Special
  • Temperature >38°C; occurs in 40% of post-op patients
  • Inflammatory response to surgical trauma; anastomotic leak; transfusion reaction; drug reaction (especially sulfa drugs)
  • Also: atelectasis (within 48 hrs), UTI, chest infection, thrombophlebitis, DVT — search for a focus
84

Postoperative Delirium / Confusion

Mng
  • Identify any correctable mechanism (e.g. pain, metabolic)
Special
  • Occurs in 50% of cases, especially elderly + orthopaedic surgery
  • A state between unconsciousness and complete wakefulness
  • Postoperative cognitive dysfunction
  • Causes: electrolyte disturbance, hypo/hyperglycaemia, acid-base disturbance, organ failure, infections, sedatives, hypoxia/hypercapnia
85

Postoperative Pneumonia (aspiration / HAP)

Mng
  • Supportive
  • Antibiotics
  • Steroids
Special
  • Aspiration of gastric contents → chemical pneumonitis → bacterial infection → soiling of lung → may lead to ARDS → high mortality
  • Retained secretions, atelectasis, pain, abdominal distension, decreased chest excursions and inability to cough
86

Perioperative Infection / Hospital-Acquired Infection (HAI)

Inves
  • Septic screen: blood cultures, FBC, CRP, midstream urine, aspiration of pus (preferred to swab), CXR
Mng
  • Support organs
  • Remove and change the lines
  • Start antibiotics (empirical vs sensitivities)
  • Don't forget infection control
Special
  • Affects 10% of in-patients; 1-4% will die; ~1/3 preventable with infection-control & antibiotic policies
  • UTI 35%, Multiple 18%, LRTI 16%, SSI 12%, Other 10%, Skin 8%, BSI 1%
  • Urine, chest, wounds & pressure sores, lines & cannulae, intra-abdominal (incl. anastomotic leaks)
87

Postoperative Pulmonary Complications (general)

Inves
  • Identification: clinical assessment, chest X-ray, sputum culture
Mng
  • Physiotherapy & mobilisation
  • Incentive spirometry
  • Close monitoring & early ICU referral
Special
  • Pre-op SaO2 <90%, age >60, obesity, pre-existing lung disease, smoking, upper-abdominal/thoracic surgery (phrenic nerve injury), prolonged surgery, general anaesthesia
  • Pre-op optimisation, physiotherapy & mobilisation, antibiotics, laparoscopic surgery, incentive spirometry

Oncology

21 entries
88

Neoplasm — definition & overview

Special
  • Mass of cells that (a) proliferate in an atypical, relentless way AND (b) serve no useful function
  • Lecturer framing — 'cancer cells are psychopaths': uncontrolled proliferation, unbounded spread; relentlessly destroy the tissue first, then the person
  • Cells divide without proper checks/balances; mutations arise constantly; mutations hitting tumour-suppressor genes inhibit apoptosis & encourage further mutations; some mutations → drug resistance
89

Cancer epidemiology

Special
  • 1 in 4 deaths in the USA is caused by cancer — second only to heart disease
  • Leading cause of death before age 65 in both sexes (USA)
  • Absolute case numbers are rising, but the death rate has been falling since the early 1990s
90

Benign vs malignant neoplasm

Special
  • Benign — cells do NOT invade surrounding tissue; remain a local conglomerate. Malignant — cells can (1) invade and (2) metastasize
91

Tumour biology — malignant cell capabilities

Special
  • Grow/proliferate in the absence of external stimuli; oncogenes (aberrant forms of normal cellular genes) are key; normal sequences — 'the seeds of our own destruction' — mutate into active oncogenes → malignant transformation
  • Normal cells divide only a finite 40–60 times, limited by progressive telomere shortening (a molecular clock); cancer cells use telomerase to rebuild the telomere each cycle → no shortening → immortality
  • Malignant transformation may be more frequent than clinical cancer; protective mechanisms = loss of transformed cells by wastage (mucosal shedding) + immune surveillance destroying them before they proliferate
  • Suppress expression of tumour-associated antigens; actively co-opt one part of the immune system to help the tumour escape detection by another part
92

Tumour invasion & metastasis

Special
  • (1) Rise in interstitial pressure from unrestrained proliferation + loss of contact inhibition; (2) dissolve ECM via collagenases/proteases (prostaglandins induce osteolysis → skeletal deposits; integrin modulation lets cells detach from ECM); (3) become mobile — abnormal integrins signal increased motility; epithelial cells behave as mesenchymal (epithelial–mesenchymal transition, EMT)
  • Migration then implantation. Migration two ways: individual cells migrate, OR embolic clumping (outer cells — sometimes normal lymphocytes — protect inner cells from immune attack). Most circulating cancer cells never form viable metastases
  • Implantation: cancer cells express inflammatory cytokines that 'fool'/activate host endothelium → activated endothelium expresses receptors binding integrins & selectins on malignant cells → they cross the endothelial barrier into extravascular space
  • Traditional: centrifugal spread → regional nodes as first step → then bloodstream. Now: malignant cells invade BOTH lymphatic and blood vessels even at the earliest stages → widespread micrometastases
  • Conceptual consequences: need for systemic treatment; radical locoregional resection challenged; regional node involvement = indicator that dissemination has occurred (not a stage); 'cure' redefined as normal life duration without clinical disease (microscopic deposits may persist)
93

Immunosuppression-associated malignancies

Special
  • Hodgkin's disease, Kaposi sarcoma, and skin / oropharynx / bone cancers
  • Non-Hodgkin's lymphoma, Kaposi sarcoma, invasive cervical cancer
  • If immune surveillance breaks down → persistence & growth of transformed cells in the host tissues
94

Clinical features of cancer

C/P
  • Local — surface lesions bleed or discharge
  • Local — hollow viscus → obstruction
  • Local — closed space → pressure
  • Local — organ failure from invasion
  • Local — severe pain from invasion; may mimic benign pain (e.g. gastric ulcer)
  • Systemic — general debility (anaemia, abnormal proteins & peptides)
  • Systemic — appropriate secretion of hormones
  • Systemic — inappropriate / ectopic secretion of hormones
Special
  • Benign tumours often remain unrecognised in life or cause symptoms from local/general effects; malignant tumours vary — some rapidly progressive & debilitating, in others local effects predominate
95

Diagnosis — imaging & biopsy

Inves
  • Radiology — plain films, contrast GI/GU studies, CT, virtual colonoscopy
  • Ultrasonography
  • Radioscintigraphy — thyroid scan, bone scan, PET & PET-CT
  • MRI — regular and dynamic enhanced MRI (DEMRI)
  • Sampling — hollow organs by endoscopy; cavities by laparoscopy / mediastinoscopy / thoracoscopy
  • FNAC — cellular pathology
  • Core needle biopsy — histological diagnosis + tissue markers
  • Incisional biopsy; excisional biopsy
Special
  • Selecting an inappropriate biopsy method can compromise subsequent surgical therapy → decision needs multidisciplinary input
  • Additional aid: measuring the frequency of cancer-specific genes gives predictive + prognostic information
96

Prognostic factors in cancer

Special
  • Beyond staging & grading, prognosis depends on additional tumour features
  • Lymphomas with cell-surface receptors for immunoglobulin respond better to chemotherapy
  • ER-positive breast cancer (cytoplasmic protein with high affinity for oestrogen) responds better to hormonal measures → better prognosis
  • Lymphocytic infiltration seen as sinus histiocytosis in regional nodes = reactive host–tumour response → better prognosis
97

Hereditary cancer syndromes — risk-reduction surgery

Mng
  • BRCA-positive without evident disease → subcutaneous mastectomy
  • Inherited CDH1 gene mutation (hereditary diffuse gastric cancer) → total gastrectomy
  • MEN2 (multiple endocrine neoplasia 2) → total thyroidectomy
  • Familial polyposis or ulcerative colitis → colectomy
Special
  • Termed risk-reduction surgery (not truly prophylactic) — one of the current roles of surgery alongside diagnostic, curative, and palliative
98

Premalignant conditions

Mng
  • Chemoprevention — tamoxifen (prevent breast cancer)
  • Chemoprevention — nicotinamide / vitamin B3 (non-melanotic skin cancer)
  • Chemoprevention — 13-cis-retinoic acid (reverse leukoplakia)
Special
  • Barrett's oesophagus — precancerous mucosal lesions treated with photodynamic therapy (PDT)
  • Actinic keratosis — premalignant skin lesion; treated with PDT
  • Leukoplakia — reversed by 13-cis-retinoic acid
  • Targeting premalignant conditions is secondary prophylaxis
99

Surgery in oncology (roles)

Mng
  • Diagnostic — LN biopsy in lymphomas; staging laparoscopy (gastric, pancreatic); mediastinoscopy (lung); laparoscopic ultrasound (avoid missing small liver tumours)
  • Curative (T) — en-bloc resection
  • Curative (N) — lymphadenectomy in oesophageal / gastric / pancreatic / colorectal; sentinel lymph node biopsy in breast & melanoma
  • Curative (M) — resect hepatic metastases of colorectal cancer; pulmonary metastases from soft-tissue sarcoma
  • Palliative (non-curative) — cytoreductive surgery, nutritional support, manage complications, vascular access for chemotherapy
  • Palliative complications managed — pain from nerve infiltration, haemorrhage, obstruction, perforated viscus
Special
  • Remove the entire tumour + any adjacent involved structures/organs; aim = a tumour-free margin → minimise local recurrence; more aggressive / poorly differentiated cancers need a wider resection margin
  • (1) adequate disease-free interval; (2) the organ of involvement; (3) ability to render the patient tumour-free with acceptable morbidity & mortality
100

Chemotherapy

Mng
  • Setting — Primary: chemotherapy alone, e.g. haematological malignancies (leukaemia, lymphoma)
  • Setting — Adjuvant: after curative surgery when high risk of relapse, e.g. node-positive breast cancer
  • Setting — Neoadjuvant: before surgery to 'downsize' the tumour → less radical operation or clear resection margin
  • Route — Systemic: oral, IV
  • Route — Regional in spaces: intraperitoneal for some GIT & ovarian tumours
  • Route — Regional via blood supply: isolated limb perfusion (extremity melanoma/sarcoma); isolated hepatic artery infusion (hepatic metastases of colorectal cancer)
101

Hormonal therapy (hormone-dependent cancers)

Mng
  • Breast cancer — surgical ablation: ovariectomy
  • Breast cancer — drugs: antioestrogen (tamoxifen), LHRH antagonist, progestogens, aromatase inhibitors (used in cases with DVT)
  • Prostate cancer — surgical ablation: orchiectomy
  • Prostate cancer — drugs: antiandrogen (flutamide), LHRH analogue, stilbosterol
102

Radiotherapy

Mng
  • Setting — Primary: alone; preferred over surgery in laryngeal, oropharyngeal cancer and facial BCC (organ/tissue preservation); e.g. seminoma, localized Hodgkin disease
  • Setting — Adjuvant: after breast lumpectomy to reduce local recurrence; cisplatin & 5-fluorouracil act as radiosensitizers
  • Setting — Neoadjuvant: downsize before surgery, e.g. rectal adenocarcinoma
  • Route — Systemic: oral radioactive iodine
  • Route — Teletherapy: external beam radiotherapy
  • Route — Brachytherapy: radiation source near or within target tissue (cervical, breast, prostate)
103

Photodynamic therapy (PDT)

Mng
  • Photosensitizer drug + a light source → free-radical (singlet oxygen) formation destroying sensitized cells
  • Singlet oxygen — (a) destroys cells directly, (b) destroys nearby blood vessels, (c) activates the immune system against tumour cells
  • Use — surface lesions: non-melanotic skin cancers, actinic keratosis
  • Use — relieve symptoms of oesophageal cancer & non-small-cell lung cancer; treat precancerous mucosal lesions in Barrett's oesophagus
104

Immunotherapy

Mng
  • Active, non-specific — BCG in superficial bladder cancer
  • Active, specific — vaccines derived from tumour cells or antigen-presenting cells
  • Passive — cytokines; interferon alpha activates natural killer cells and dendritic cells
105

Biologic / targeted therapy

Mng
  • Drugs/agents that block cancer growth & spread by interfering with specific molecules in tumour growth
  • (a) inhibit growth-factor receptors (HER2 in some breast cancers)
  • (b) inhibit intracellular signal transduction
  • (c) inhibit the cell cycle
106

Gene therapy

Mng
  • Introduces DNA or RNA into living cells to alter the genetic program of cancer cells
  • (a) replace an altered tumour-suppressor gene
  • (b) introduce genetic material to block tumour oncogene expression
107

Multidisciplinary team (MDT)

Special
  • The MDT delivers active treatment; its modalities = surgery, chemotherapy, hormonal therapy, radiotherapy, photodynamic therapy, immunotherapy, biological therapy, gene therapy
108

Palliative & end-of-life care

Mng
  • Rehabilitation/palliative care is distinct from end-of-life care; palliatively-treated patients may survive several years, whereas end-of-life care concerns the last few months of life
  • Therapeutic — local/systemic therapy to induce tumour regression: radio- & chemotherapy; surgery (excise fungating tumour, manage dysphagia / intestinal obstruction / impending paraplegia)
  • Non-therapeutic (relieves symptoms, no effect on tumour) — pain, dysphagia (tube stenting) & moniliasis, dyspnoea, vomiting, lack of sleep; physiotherapy, occupational & speech therapy
  • Non-therapeutic support — counselling/emotional, nutritional (advice & supplements), social (patients, relatives, carers), financial (entitlements, charity grants), spiritual
Special
  • Spiritual need; profound fear; specific needs of those facing bereavement — aim is a 'good death', preferably at home

Surgical Nutrition

15 entries
109

Perioperative & Postoperative Nutritional Support

Inves
  • Acute pancreatitis: follow up by Ranson's criteria every 48 hours
  • Dynamic / contrast-enhanced CT of pancreas starting ~1 week after presentation -> detect fluid collections / pancreatic necrosis and whether it becomes infected
Mng
  • No support needed -> IV fluids with appropriate electrolytes + minimum 100 g glucose daily to minimize protein catabolism
  • Normal protein 0.8 g/kg/day (unstressed); normal energy 20 kcal/kg/day
  • Moderate stress: protein 1.2-1.4 g/kg/day. Severe stress: protein 1.5-2 g/kg/day. Sepsis calorie stress factor 1.3-1.35
  • Route ladder: oral diet/supplements -> enteral (nasojejunal tube; elemental / blendarized / polymeric nutritionally-complete formula) -> IV hyperalimentation / TPN; enteral route resorted to whenever possible
  • Even most score-3 cases: increased protein covered by oral diet or supplements; fast-track (ERAS) + early enteral nutrition recommended in GIT surgery
  • Persistent vomiting (e.g. acute pancreatitis / benign gastric outlet obstruction): nasojejunal tube to deliver blendarized/elemental formula beyond the outlet
  • Crohn's ileocolic fistula: elemental diet via nasojejunal tube facilitates jejunal nutrient absorption despite complicating diarrhoea
  • Cirrhotic/hepatic: modular formulation for hepatic disease on resuming oral feeding; early postop IV hyperalimentation may aid anastomotic/wound healing
  • Emergency/hypovolaemic sequence: resuscitate (fluid + electrolytes, combat metabolic acidosis) -> control source of infection/sepsis (amputation, resection of gangrenous loops, debridement which may be repeated) -> then nutritional support (gradual IV hyperalimentation / TPN)
Special
  • Majority do NOT — most have adequate fuel reserves to withstand common catabolic stresses and partial starvation for at least one week
  • Gastrostomy NOT advisable — adhesions complicate a future colon bypass / interfere with stomach mobilization for the planned surgery; stenting a tight stricture may be difficult/dangerous (risk of perforation)
  • Successful stenting improves nutrition AND avoids saliva overflow/aspiration into the airway (aspiration of saliva = disadvantage of a feeding gastrostomy)
110

Marasmus / Protein-Energy Malnutrition (PEM)

C/P
  • Weight loss with erosion of muscle and fat stores
Special
  • Inadequate intake of an otherwise balanced diet OR impaired delivery
  • No food / no appetite (depression, medications, dementia) + GI dysfunction
  • COMPENSATED protein catabolism; normal or reduced metabolic rate
111

Kwashiorkor

C/P
  • Characteristic FLUID RETENTION that masks the often rapid erosion of muscle and fat stores
Special
  • Inadequate AND unbalanced diet (relatively more calories than protein) OR impaired utilization
  • Sepsis, major trauma, burns
  • UNCOMPENSATED protein catabolism; INCREASED metabolic rate
112

Cachexia

C/P
  • Profound loss of adipose and skeletal muscle mass with haematological derangement and deconditioning
Special
  • Interplay of altered metabolism and inflammation
  • Metabolic disease, cancer, AIDS (TNF-alpha), end-stage organ disease
  • Cancer-induced anorexia; host cytokine production (TNF); rise in resting energy expenditure; tumour retains nitrogen and runs a glucose-wasteful, high-rate anaerobic metabolism
  • Uncompensated protein catabolism; increased metabolic rate
113

Sarcopenia

C/P
  • Loss of muscle mass AND quality manifesting as frailty with decreased strength
Special
  • Reduced androgenic hormones, rising insulin resistance, decreased exercise and decreased protein intake
  • Ageing
  • Uncompensated protein catabolism; normal/reduced metabolic rate
114

Nutritional Support — Rationale & Indications

Mng
  • General indications: (1) significant PCM pre-operatively; (2) well-nourished patient undergoing a major operation; (3) well-nourished patient subjected to major trauma
Special
  • Prevent or reverse the catabolic effects of disease/injury; ultimate validation = improved clinical outcome and restored function
  • No — most have fuel reserves to withstand catabolic stress/partial starvation for at least 1 week; IV fluids + electrolytes + a minimum of 100 g glucose daily (to minimize protein catabolism) is adequate
  • Deficient intake (voluntary, anorexia nervosa, starvation — repeated vomiting/elderly/deficient teeth/poverty); malabsorption (coeliac sprue, Whipple, TB enteritis; stagnant loop — jejunal diverticulitis, Crohn's fistula; postop short bowel/stagnant loops); metabolic (autoimmune disease, malignancy ± cachexia)
115

Enteral Nutrition

Mng
  • Indication: functional GI tract but unable to sustain an adequate oral diet
  • Contraindications (mostly relative/temporary): intestinal obstruction, ileus, vomiting, high-output enterocutaneous fistula, diarrhoea, enterocolitis
  • Feeding tubes: nasogastric, nasojejunal, gastrostomy, jejunal — jejunal preferred for long-term access and requires CONTINUOUS (not bolus) infusion
  • Formulae: polymeric (blenderized/nutritionally complete); elemental (chemically defined, hyperosmolar); modular (pulmonary/hepatic/renal/immunodysfunction)
Special
  • Enteral preferred — lower cost, avoids IV/vascular-access complications; post-op enteral nutrition reduces infectious complications and acute-phase protein production in GI surgery
116

Parenteral Hyperalimentation (PPN / TPN)

Mng
  • Indications: newborns with catastrophic anomalies (TE fistula, gastroschisis, omphalocele, massive intestinal atresia); infants failing to thrive / short bowel / malabsorption / enzyme deficiency / meconium ileus / idiopathic diarrhoea; adult short bowel; normal bowel length with malabsorption (intestinal/pancreatic); enteric fistula; prolonged paralytic ileus after major ops (7–10 days); functional GI disease (oesophageal dyskinesia post-CVA, anorexia nervosa, psychogenic vomiting); critically ill hypermetabolic >5 days; failed enteral feeding/high residuals; granulomatous/ulcerative colitis or TB enteritis with diseased mucosa; malignancy ± cachexia
  • Contraindications: haemodynamic instability/severe metabolic derangement needing correction before hypertonic fluid; no hope of meaningful life (only delaying death); irreversibly decerebrate/dehumanized; infants with <8 cm small bowel; good nutritional state; GIT feeding feasible
  • Delivery catheters: peripheral (PPN) or central (TPN)
  • TPN solutions: 3-in-1 admixture (protein/carb/fat); 2-in-1 with lipid emulsion given separately; special low/intermediate/high protein-nitrogen formulas for diabetes/renal failure/hepatic dysfunction; may be continuous or cyclic
  • Cyclic TPN (8–16 h at night): patients discharged on home TPN; limited IV access needing other meds (e.g. chemotherapy); metabolically stable patients wanting a pump-free daytime period
  • Nutrient solution: surgeon prescribes daily energy, daily protein, water/electrolytes/vitamins/trace metals; pharmacist mixes all in a 3-litre bag infused over 24 h
  • Introduction is GRADUAL: ~1000 kcal on day 1, then +500 kcal/day increments if metabolically stable (e.g. normoglycaemia) until the caloric goal is reached
Special
  • Continuous infusion of a HYPEROSMOLAR solution (carbohydrates, proteins, fats, nutrients) via an indwelling catheter preferably placed in the superior vena cava
117

TPN — Common Metabolic Complications

Mng
  • Hyperglycaemia — too-rapid infusion / developing sepsis → slow rate, add insulin, treat sepsis
  • Hypoglycaemia — rapid cessation of nutrient fluid → give 10% dextrose for 8 h when stopping
  • Hypertriglyceridaemia — too much fat → discontinue fat infusion
  • Hyperchloraemic metabolic acidosis — too much chloride → give Na and K as acetate salts
  • Prerenal azotaemia — excessive amino acid infusion → reduce intake or increase free water
  • Hypophosphataemia — insufficient phosphorus → ensure 20 mmol phosphate per 1000 kcal
  • Hypokalaemia — depleted patient/insufficient K → slow administration and add more K
  • Hyperkalaemia — metabolic acidosis, renal failure → stop all intake and treat the cause
118

Immunonutrition

Special
  • Conditional amino acid — stimulates immune cells, NO precursor improving microvascular perfusion → may decrease infection, reduce length of stay
  • Maintain cell membranes, modulate inflammation → decreased mortality, clinically safe
  • Conditional amino acid (70% of AA mobilised during stress) — antioxidant, glutathione precursor, energy for enterocytes → may decrease infection, reduce LOS, improve QoL, nitrogen balance and sugar control
119

Nutritional Assessment — Clinical Parameters

C/P
  • History weight-loss thresholds: 5% in the last month / 10% over 6 months / 80–85% of ideal body weight
  • GIT symptoms: poor appetite, vomiting, diarrhoea; generalized muscle weakness; unhealed scratches/sores
  • Fat depot: loss of subcutaneous fat (triceps skin fold)
  • Protein depot — muscle wasting: thenar, temporal, quadriceps, deltoid (mid-arm circumference)
  • Visceral protein: hypoproteinaemia → peripheral/presacral oedema and ascites
  • Subtle deficiency signs: skin rash, pallor, glossitis, gingival lesions, hair changes, hepatomegaly, neuropathy, dementia
120

Nutritional Assessment — Laboratory Markers

Inves
  • Serum albumin <3 g/dl in a stable hydrated patient; half-life 14–20 days
  • Serum prealbumin (thyroxine-binding): shorter half-life 2–3 days; MORE accurate for nutritional assessment
  • Serum transferrin <200 mg/dl; half-life 8–10 days
121

Nutritional Assessment — Physical Performance

Inves
  • Hand grip: squeeze against the surgeon's index + middle finger for 10 seconds (compare by age/sex/habitus) or hand-held vigorimeter (objective)
  • Respiratory-muscle testing: shortness of breath at rest = moderate impairment; unable to hold a normal conversation = severe
  • Clinical test: blowing a paper 10 cm from the lips
122

Energy Metabolism & Body Composition

Special
  • Glucose (carbohydrates), amino acids (proteins), fatty acids (lipids), ketone bodies
  • Fat 14 kg = 125,000 kcal; protein 12 kg (skeletal muscle 6 kg + other 6 kg) = 48,000 kcal; carbohydrate — muscle glycogen 600, liver glycogen 300, free glucose 80 kcal
  • Proteins, water, energy, electrolytes (Na/K), minerals (Ca/P/Mg) + trace elements (Cu/Fe/Se/Zn), vitamins (water- and fat-soluble)
123

Body Water & Malnutrition Epidemiology

Special
  • 55–60% of body mass (40 L): intracellular 22 L; extracellular = interstitial 14 L + plasma 3–3.5 L
  • Loss of body fat, ECF compartment expansion (oedema), loss of lean body mass
  • ~half of hospitalized patients are malnourished or at risk; severe PCM in 1 in 10; malnourished surgical patients have higher mortality and are 2–3× more likely to develop complications (longer stay, higher cost)

Trauma (ATLS)

10 entries
124

Trauma (introduction / epidemiology)

Special
  • WHO identifies trauma as the major healthcare challenge of our century; estimates major-trauma mortality in Europe could fall 30% by improving the chain of care.
125

ABCDE Primary Survey (trauma)

Mng
  • Exposure/logroll: high priority in penetrating trauma (stab/gunshot); may be postponed in cardiovascularly unstable blunt trauma when pelvic or spinal injury suspected.
Special
  • Taught as <c>ABCDE — a preceding 'c = catastrophic haemorrhage' step comes BEFORE Airway.
126

ATLS Haemorrhage Classification (4-Stage)

Special
  • Base deficit: Class I 0 to −2 mEq/L; II −2 to −6; III −6 to −10; IV −10 mEq/L or less.
  • Need for blood: I monitor; II possible; III yes; IV Massive Transfusion Protocol. BP only tanks in Class IV — a hypotensive trauma patient is always Class IV.
127

Tension pneumothorax

Special
  • One of the 6 immediately life-threatening thoracic conditions to exclude/treat in the Breathing (B) step.
128

Cardiac tamponade

Special
  • One of the 6 immediately life-threatening thoracic conditions to exclude/treat in Breathing (B); flagged as an SBA in the lecture.
129

Massive haemothorax

Special
  • One of the 6 immediately life-threatening thoracic conditions to exclude/treat in the Breathing (B) step.
130

Flail chest

Special
  • One of the 6 immediately life-threatening thoracic conditions to exclude/treat in the Breathing (B) step.
131

Open (sucking) chest wound

Special
  • One of the 6 immediately life-threatening thoracic conditions to exclude/treat in the Breathing (B) step.
132

Laryngo-tracheal injury

Special
  • One of the 6 immediately life-threatening thoracic conditions to exclude/treat in the Breathing (B) step.
133

Traumatic cardiac arrest

Special
  • Named on the Breathing slide alongside the six life-threatening thoracic conditions (reversible causes to exclude).

External Herniae

10 entries
134

External abdominal hernia (definition)

Special
  • Latin 'hernia' = 'a rupture'
  • Abnormal protrusion of an organ/tissue through an orifice (natural or induced) in its surrounding space
  • May occur between two adjacent cavities — e.g. abdomen and thorax
  • Most commonly develops through the abdominal wall
  • Pancreas — the only intra-abdominal organ that does not protrude through an abdominal-wall defect (posterior retroperitoneal position)
  • Hernia repair = single most common operation performed by a general surgeon
  • Usually has a peritoneal sac protruding through an aperture in the fascia transversalis
  • Groin (inguinal ± femoral) vs Ventral
135

Indirect inguinal hernia

Special
  • Lateral to the inferior epigastric vessels — through the deep (internal) inguinal ring, lateral to Hesselbach's triangle
  • A persistent/patent processus vaginalis — a congenital preformed hernia sac
  • Follows the spermatic cord through the canal → superficial ring → can reach the scrotum
  • Inguinal hernia 'develops as a tribute to the descent of the testis to the scrotum'
136

Direct inguinal hernia

Special
  • Medial to the inferior epigastric vessels — through Hesselbach's (inguinal) triangle
  • Through the weak transversalis fascia within the inguinal triangle
  • Acquired
137

Femoral hernia

Special
  • Through the femoral canal, below the inguinal ligament
  • Femoral canal = medial-most compartment of the femoral sheath; femoral vein laterally, lacunar ligament medially
  • Superior to Cooper's ligament, inferior to inguinal ligament, medial to femoral vein, lateral to lacunar ligament
  • 'Develops as a tribute of standing up on the lower limbs in Homo sapiens'
  • Sac may turn upward over the inguinal ligament (along the superficial epigastric vein) → mimics an inguinal hernia on exam
  • Bilocular sac can result from an aberrant obturator artery
138

Ventral hernia

Special
  • Through the midline aponeurotic zone (linea alba) — in contrast to the groin hernias
  • One of the two major hernia groups (Groin vs Ventral)
139

Epigastric hernia

Special
  • Defect produced where a diaphragmatic tendinous slip intermingles with the posterior slip of the 2nd tendinous intersection of rectus abdominis
140

Hydrocele (and processus vaginalis anomalies)

Special
  • Processus vaginalis narrowed but its lumen still communicates with the abdominal cavity → peritoneal fluid accumulates in it
  • Upper and lower ends of the processus obliterated, leaving a small intermediate cystic area
  • Fluid within the tunica vaginalis; can follow inflammation of the testis; most hydroceles are idiopathic
  • Scrotal hydrocele: patent processus lets peritoneal fluid pass into the tunica vaginalis; often with swelling of the spermatic cord; both appear/disappear in a gravity-dependent manner
141

Cryptorchidism (undescended testicle)

Special
  • Common congenital defect in males — a testicle not fully descended into the scrotum via the inguinal canal, sitting somewhere along the normal descent route
  • Inguinal canal
  • 1 intra-abdominal; 2 deep inguinal ring; 3 inguinal canal (most common); 4 superficial inguinal ring
142

Ectopic testicle

Special
  • Descends through the inguinal canal normally, then deviates to a non-scrotal location
  • Anterior abdominal wall, upper-medial or anterior thigh, perineum, or opposite scrotum/groin region
143

Canal of Nuck

Special
  • Persistence of the processus vaginalis in the female (rare)
  • The female processus vaginalis is normally small and quickly disappears
  • Swelling in the inguinal canal or in the proximal/anterior labia majora

Surgical Safety

3 entries
1

WHO Surgical Safety Checklist (3 Phases)

  • Sign In (before induction): identity, site, consent, pulse ox, allergies, airway risk
  • Time Out (before skin incision): team intro; antibiotic prophylaxis (<60 min); critical events anticipated
  • Sign Out (before patient leaves): instrument/needle counts; specimen labelling
2

Enhanced Recovery After Surgery (ERAS)

Goal: Reduce surgical stress to retain anabolic homeostasis.

Key elements
  • Carbohydrate drinks 2 hours before surgery (replaces overnight fasting)
  • Minimally invasive approaches
  • Fluid management (balance vs large volumes)
  • Early removal of drains/tubes
  • Early mobilisation
  • Serving drinks/food day of operation
Outcomes
  • Shorter hospital stay (30–50%)
  • Reduced complications
  • Reduced cost
3

SSI Prevention Bundle

  • Antimicrobial prophylaxis — 5 sub-elements: name; timing; weight-based dose; re-dosing; discontinuation
  • Skin antisepsis — standardised peri-operative practices
  • Temperature control — normothermia maintenance
  • Glycaemic control — glucose control optimisation
  • Oxygenation — supplemental oxygen
  • MRSA — screening/decolonisation
  • Aseptic measures — traffic control; attire; audit

Pain & Sedation

4 entries
4

WHO Analgesic Ladder

  • Step 1: Non-opioid ± adjuvant
  • Step 2: Opioid for mild to moderate pain ± non-opioid ± adjuvant
  • Step 3: Opioid for moderate to severe pain ± non-opioid ± adjuvant

Golden Rule: Treat the PATIENT, not the number.

5

SOCRATES (Pain History Mnemonic)

  • S — Site
  • O — Onset (sudden/gradual)
  • C — Character
  • R — Radiation
  • A — Associations
  • T — Time course (pattern)
  • E — Exacerbating/Relieving factors
  • S — Severity
6

FLACC Scale (Paediatric / Non-verbal)

Use: Pain assessment in children or non-verbal patients. Total score 0–10 (Merkel et al, 1997).

CategoryScore 0Score 1Score 2
FaceNo particular expression or smileOccasional grimace or frown, withdrawnFrequent/constant frown, quivering chin, clenched jaw
LegsNormal position or relaxedUneasy, restless, tenseKicking or legs drawn up
ActivityLying quietly, normal position, moves easilySquirming, shifting back and forth, tenseArched, rigid, or jerking
CryNo cry (awake or asleep)Moans or whimpers; occasional complaintCrying steadily, screams or sobs, frequent complaints
ConsolabilityContent, relaxedReassured by touching, hugging, talking; distractibleDifficult to console or comfort
7

Pain Assessment Tools

Frequency: Every time vital signs are taken.

Physiological
  • Autonomic (BP, HR, RR), cortical level
Patient reporting
  • Verbal: "mild" / "moderate" / "severe"
  • Visual Analogue Scale (10 cm line)
  • Verbal Numerical Rating Scale (0–10)
  • Wong-Baker FACES: 0 (No Hurt) to 10 (Hurts Worst)
Protocol
  • Assess — Treat — Reassess — Escalate

Post-op

3 entries
8

4 Ws of Post-op Fever

Use: Systematic check for principal sources of postoperative fever. Fever = temperature >38°C (occurs in ~40% of post-op patients).

  • Wind — atelectasis or pneumonia
  • Water — urinary tract infection
  • Walk — thrombophlebitis
  • Wound — wound infection
Work-up
  • Look at surgical incisions
  • Look at IV sites for septic thrombophlebitis
  • Order blood/urine/sputum cultures
  • Obtain chest X-ray if breath sounds worrisome

Early causes (1–3 days): atelectasis (traditional). Late causes (~2 weeks): septic thrombophlebitis (from IV line); occult intra-abdominal abscesses.

9

PINCH ME (Delirium Causes)

Use: Mnemonic for correctable causes of postoperative delirium. Postop delirium ~50% of cases (especially elderly + orthopaedic surgery).

  • P — Pain
  • IN — Infection
  • C — Constipation
  • H — Dehydration
  • M — Medications
  • E — Environment

Other causes to consider: electrolyte disturbance, hypo/hyperglycaemia, acid-base disturbance, organ failure, sedatives, hypoxia or hypercapnia.

10

Tetanus Prophylaxis Algorithm

Tetanus-prone wound criteria (any of)
  • Sustained >6 hours before surgery
  • Significant devitalised tissue
  • Puncture injury
  • Contact with soil/manure
  • Associated clinical sepsis, foreign body, or compound fracture
Management by vaccine status
Vaccine statusWound typeAction
Up to dateStandardNo further vaccine
Up to dateHigh risk (e.g., manure)+ Human tetanus immunoglobulin
Not up to dateTetanus-proneReinforcing Td/IPV + Immunoglobulin
Not up to dateNon-proneReinforcing Td/IPV only (or start course)
Immunoglobulin dose
  • Standard: 250 IU IM
  • High risk / >24h elapsed / heavy contamination / burns: 500 IU

Stress & Metabolic Response

17 entries
11

Ebb & Flow phase model (Cuthbertson / Moore)

Use: Biphasic metabolic model of the stress response to injury

Origin
  • First referenced by Sir David Cuthbertson (1930s) from observations of a biphasic immune, inflammatory + metabolic response to injury
  • Further modified by Francis Moore (1970s)
Ebb phase
  • Early (<24 h), HYPOmetabolic; metabolic rate falls below normal; directed at immediate survival
Catabolic flow phase
  • HYPERmetabolic (supranormal); proteolysis + lipolysis for hepatic gluconeogenesis; catabolism peaks ~48-72 h post-injury
Anabolic flow phase
  • HYPERmetabolic recovery; surges in insulin, GH + IGF-I within 5-10 days; metabolic rate returns to normal
Chronic critical illness variant
  • Classic ebb-and-flow altered; recurrent sepsis / proinflammatory stimuli -> fluctuating demand that remains chronically elevated
12

Influence of injury severity on resting metabolism (%REE)

Use: Peak resting energy expenditure (%REE) by injury type (peaks ~days 10-12 post-injury)

  • Major burns ~205% REE
  • Sepsis / peritonitis ~165%
  • Skeletal trauma ~133%
  • Elective surgery ~118% (top of normal range)
  • Starvation ~70% (below normal)
  • Normal REE = shaded band (~90-115%)
13

Injury severity vs nitrogen wasting (g/day)

Use: Peak daily nitrogen excretion by insult

  • Major burns ~28 g/day
  • Skeletal trauma ~21 g/day
  • Severe sepsis ~18 g/day
  • Infection ~15 g/day
  • Elective surgery ~11 g/day
  • Partial starvation ~4 g/day
  • Total starvation ~1.5 g/day
  • Normal shaded band ~7-10 g/day
14

Toxic factors initiating / modifying the stress response

Use: Classification of toxic factors in the stress response

Endogenous
  • Particulate: fat emboli, small platelet aggregations - modify the response
  • Non-particulate (from injured / hypoxic area): ATP, kinin, myoglobin
Exogenous
  • Endotoxin or exotoxin - initiate shock
15

Factors initiating the stress response to surgery (intra- vs post-operative)

Use: Intra- vs post-operative triggers of the surgical stress response

Intraoperative
  • Anaesthesia (hypotensive anaesthesia, drugs)
  • Emergency surgery (original disease + reperfusion injury)
  • Depletion of the circulating volume
Postoperative
  • Pain
  • Inflammatory response (control of injury + preparation for healing)
  • Toxic factors
16

Types of Shock — Haemodynamic Profile

Use: compare shock types across haemodynamic parameters

Parameters compared
  • Heart Rate
  • Blood Pressure
  • CVP
  • SVR
  • Cardiac Output
  • PCWP
  • SvO2
  • (CaO2–CvO2)
  • VO2
Shock types in the table
  • Hypovolaemic (early / late)
  • Cardiogenic
  • Neurogenic
  • Septic (hypovolaemic)
  • Septic (euvolaemic)
  • Obstructive
Neurogenic profile
  • HR normal or ↓
  • BP ↓
  • CVP ↓
  • SVR ↓
  • CO ↓
Obstructive profile
  • HR ↑
  • BP ↓
  • CVP ↑
  • SVR ↑
  • CO ↓
17

Metabolic Substrate Response Table

Use: substrate handling by metabolic state (fed / starvation / trauma & operations / sepsis)

Fed state
  • carbohydrate 30–40% of calories
  • fat 25–45% of calories
  • protein 15% of calories (45% structural / not exchangeable, 55% circulating or in cells)
Starvation
  • low CHO stores act as rapid glucose provider for the brain
  • over several days ketone bodies from fat as brain fuel (keto-adaptation)
  • keto-adaptation preserves muscle protein
Trauma & operations
  • systemic inflammatory response occurs
  • glycogen catabolised → increase glucose
  • keto-adaptation does NOT occur
  • fats catabolised → ↑ glucose + FFA in circulation, ↓ in periphery
  • protein catabolised → glucose + amino acids for immune response & healing → muscle mass loss → impaired functional recovery
Sepsis
  • systemic inflammatory response occurs
  • keto-adaptation does NOT occur
  • severe sepsis + burns → protein catabolism even more marked + energy expenditure massively increases, fuelled by intense FFA oxidation
18

Fluid Shift After Haemorrhage — Severity Classification

Use: classify capillary/osmotic/membrane forces and net restitution by haemorrhage severity

Minimal haemorrhage
  • capillary hydrostatic forces increase
  • extracellular osmolality effect minimal
  • cell-membrane dysfunction none
  • net: restitution of blood volume
Moderate haemorrhage
  • capillary hydrostatic → transcapillary refill of intravascular space
  • extracellular osmolarity → expansion of extracellular volume
  • cell-membrane dysfunction minimal
  • net: partial restitution of blood volume
Severe haemorrhage
  • capillary hydrostatic effects decrease
  • extracellular osmolarity effect none
  • cell-membrane dysfunction → influx of sodium and fluid into cells
  • net: intracellular fluid sequestration, minimal restitution of blood volume
19

Factors Initiating the Surgical Stress Response

Use: intraoperative vs postoperative triggers of the surgical stress response

Intraoperative
  • anaesthesia (hypotensive anaesthesia, drugs)
  • emergency surgery (original disease + reperfusion injury)
  • depletion of the circulating volume
Postoperative
  • pain
  • inflammatory response (control of injury, prepare for healing)
  • toxic factors
Toxic factors
  • endogenous particulate: fat emboli, small platelet aggregations (modify the response)
  • endogenous non-particulate from injured/hypoxic area: ATP, kinin, myoglobin (modify)
  • exogenous: endo- or exotoxin (initiate shock)
20

Tissue-Injury Source Classification

Use: classify the sources of tissue injury

Trauma
  • mechanical: penetrating, blunt, blast
  • chemical
  • burns (highest level of hypermetabolism)
Surgery
  • elective
  • emergency
Infection
  • primary cause of injury
  • secondary complication of other injuries (highest level of protein catabolism)
Others
  • autoimmunity
  • ischaemia
21

Ebb and Flow model of the stress response (Cuthbertson, 1930)

Use: Two-phase model of the metabolic recovery process after injury.

Three phases
  • Ebb (early) phase = a 'holding pattern' within the first 12 h, clinically manifests as SHOCK, HYPOmetabolic
  • Catabolic flow phase = HYPERmetabolic, lasting several days
  • Anabolic (recovery/repair) flow phase = HYPERmetabolic, lasting several weeks
  • duration depends on the extent of initial injury + any ongoing insults
Ebb and flow revisited (chronic critical illness)
  • in chronically critically ill patients the classic ebb-and-flow is lost
  • recurrent sepsis / proinflammatory stimuli produce a fluctuating, chronically elevated metabolic demand
22

Starvation vs Stress metabolic comparison

Use: Row-by-row contrast of simple starvation vs the stressed metabolic state.

Starvation vs Stress
  • Resting energy expenditure: decreased vs increased
  • Mediator activation: NA vs +++
  • Primary fuel: fat vs mixed
  • Proteolysis: + vs +++
  • Branched-chain oxidation: + vs +++
  • Hepatic protein synthesis: + vs +++
  • Ureagenesis: + vs +++
  • Urinary nitrogen loss: + vs +++
  • Glucogenesis: + vs +++
  • Ketone body production: ++++ vs +
23

Two-event (bimodal) model of MODS / MOF

Use: How multi-organ dysfunction develops after injury.

  • initial priming insult + sequential second hit during the vulnerable period -> dysfunctional hyperinflammation
  • early peak: within 3 days of the initial insult
  • late peak: 6-8 days after the insult
24

Influence of injury severity on resting energy expenditure (%REE)

Use: Approximate peak resting energy expenditure vs normal by insult.

  • major burns ~205%
  • sepsis / peritonitis ~165%
  • skeletal trauma ~132%
  • elective surgery ~118%
  • starvation falls to ~68%
25

Nitrogen-wasting by injury severity

Use: Approximate peak urinary nitrogen loss (g/day) by insult.

  • major burns ~28
  • skeletal trauma ~21
  • severe sepsis ~18
  • infection ~15
  • elective surgery ~11
  • partial starvation falls to ~4
  • total starvation to ~1.5
26

'SO' framework - secondary insults to avoid (3 Is)

Use: Modifiable drivers that worsen the stress response - avoid for speedy resolution.

  • Ischaemia
  • Infection
  • Inadequate oxygenation (hypoxia)
  • plus ongoing trauma e.g. compartment syndrome (abdominal / limb)
27

Hinchey grade 4 (perforated diverticular disease)

Use: Severity of perforated diverticular disease (Case 7 community-acquired severe sepsis).

  • grade 4 = perforated diverticulitis with generalized faeculant peritonitis

Surgical Nutrition

11 entries
28

How to Proceed in Nutritional Assessment (stratification algorithm)

Use: Order of stratification when assessing perioperative nutritional risk.

1) Age
  • Age first (age >70 adds 1 to score)
2) Benign pathology (trauma, peritonitis, benign strictures, non-malignant fistulae)
  • ICU or not
  • Diabetic or not
  • Comorbid with acute complication
  • Hip fractures
  • Impaired nutrition or not — if impaired, short- or long-term duration
  • Scheduled for major or minor surgery
3) Malignant pathology
  • Long-term nutritional derangement (score 1, 2 or 3)
  • Specific conditions: haematological malignancy (score 2); bone marrow transplantation (score 3)
  • Scheduled for major or minor (palliative) surgery — major = score 2
29

Nutritional Risk Screening (NRS 2002)

Use: Two-part nutrition screening tool for hospitalized/surgical patients

Part A — Initial screening (4 questions)
  • (1) Is BMI <20.5?
  • (2) Has the patient lost weight within the last 3 months?
  • (3) Reduced dietary intake in the last week?
  • (4) Is the patient severely ill (e.g. in intensive care)?
  • If YES to any → proceed to Part B; if NO → rescreen weekly
Part B — severity-of-disease scoring
  • Score 1: chronic disease admitted for complications; weak but out of bed; protein need increased but coverable by oral diet/supplements
  • Score 2: confined to bed, e.g. post major abdominal surgery; protein need substantially increased, artificial feeding often required
  • Score 3: intensive care with assisted ventilation; protein need cannot be covered even by artificial feeding
  • Nutritional status threshold: wt loss >5% in 2 months, or BMI 18.5–20.5 with impaired general condition, or food intake 25–60% of requirement in the preceding week
Age adjustment
  • If age >70, add 1 → age-adjusted total score
Interpretation
  • Total score ≥3 = nutritionally at-risk → initiate a nutritional care plan
  • Total score <3 = weekly rescreen (consider a preventive plan if scheduled for a major operation)
Source
  • Kondrup J, Allison SP, Elia M, Vellas B, Plauth M. ESPEN guidelines for nutrition screening. Clin Nutr 2003;22:415–21
30

Prognostic Nutritional Index (PNI)

Use: Predicts risk of complications from nutritional status

  • PNI = 158% − 16.6(albumin) − 0.2(transferrin) − 0.78(triceps skin fold in mm) − 5.8(delayed-hypersensitivity score)
Risk
  • >50% = high risk for complications
  • 40–49% = intermediate risk
  • <40% = low risk
31

Delayed-type Hypersensitivity Scoring (for PNI)

Use: Skin-antigen induration score feeding into the PNI

  • >5 mm induration = score 2
  • >1–5 mm induration = score 1
  • Anergy = score 0
32

Total Lymphocyte Count (TLC) Depletion

Use: Grades immune/nutritional depletion

  • TLC = %lymphocytes × WBC / 100
  • Mild depletion 1500–1800/mm³
  • Moderate depletion 900–1500/mm³
  • Severe depletion <900/mm³
33

BMI Classification (nutritional)

Use: Classifies weight-for-height / degree of malnutrition

  • BMI = weight (kg) / height² (m)
  • <18.4 = underweight (suggestive of severe protein-calorie malnutrition)
  • 18.5–24.9 = ideal weight for height
  • 25–29.9 = over ideal weight
  • 30–39.9 = obese
  • >40 = very obese
34

Harris-Benedict Basal Energy Expenditure (BEE)

Use: Estimates daily basal energy expenditure (kcal/day)

  • Men: BEE = 66.4 + (13.7 × wt kg) + (5 × ht cm) − (6.7 × age yr)
  • Women: BEE = 655 + (9.6 × wt kg) + (1.8 × ht cm) − (4.7 × age yr)
  • Unstressed ≈ 20 kcal/kg/day
35

Protein Requirements by Metabolic Stress

Use: Daily protein target by stress level

  • Unstressed 0.8 g/kg/day
  • Mild stress 1.0–1.10 g/kg (elective hospitalization)
  • Moderate stress 1.2–1.4 g/kg (complicated post-op care/infection)
  • Severe stress 1.5–2.5 g/kg (major trauma, pancreatitis, sepsis)
  • Calorie:nitrogen ratio ≈ 150:1
36

Caloric Requirements & Stress Factors

Use: Adjusts baseline calorie need by degree of stress

  • Normally 20 kcal/kg/day
  • Starvation stress factor 0.8–1.0
  • Elective operation 1–1.1
  • Sepsis 1.3–1.35
  • Burn 1.3–1.5
37

Catabolic Index (CI) & Creatinine-Height Index (CHI)

Use: Additional nutritional indices (alongside BMI and PNI)

  • Catabolic Index (CI)
  • Creatinine-Height Index (CHI)
  • Named as additional nutritional indices alongside BMI and PNI
38

Markers of Metabolic Stress

Use: Clinical/lab flags of a metabolic stress state

  • Highest temperature in the last 24 h >100°F
  • Pulse >100/min in the last 24 h
  • Respiratory rate >30/min in the last 24 h
  • WBC >12,000 or <3,000 in the last 24 h
  • Positive blood culture
  • Active inflammatory bowel disease
  • Defined focus of infection

Oncology

12 entries
39

TNM / pTNM staging

Use: Formal cancer staging to predict prognosis and select the correct treatment.

  • Clinical staging = pretreatment T N M system
  • Postsurgical histopathological staging = pTNM
  • Staging aids prediction of prognosis and determines correct treatment
  • For some cancers, staging also incorporates histological grading of the primary tumour
40

Histological grading (G1–G3)

Use: Degree of tumour differentiation; feeds into staging & prognosis.

  • G1 — well differentiated (low grade)
  • G2 — moderately differentiated (intermediate grade)
  • G3 — poorly differentiated / anaplastic (high grade)
41

Neoplasm classification schema

Use: Three axes used to classify any neoplasm.

Cell of origin
  • Epithelium → adenoma / adenocarcinoma
  • Mesenchymal / connective tissue → '-oma' or sarcoma
Tissue of origin
  • Skin
  • Breast
  • GIT
  • Lung
  • Urogenital
  • Haematological
  • Nervous system
Gross appearance
  • Cauliflower mass
  • Ulcerating
  • Fungating
  • Spreading (superficial or submucosal)
  • Cicatrizing
42

Hallmarks / functional capabilities of malignant cells

Use: Organising framework of malignant cell biology.

Growth capabilities
  • Self-sufficient growth
  • Limitless replication (immortality)
Anti-growth factor evasion
  • Insensitivity to anti-growth signals
  • Evasion of apoptosis
Interaction with other elements
  • Sustained angiogenesis
  • Sustained tissue invasion
43

Aetiology classification (exogenous vs endogenous)

Use: Most cancers = a complex combination of exogenous and/or endogenous factors, not a single physical/chemical/biological factor.

Exogenous factors
  • Physical
  • Chemical
  • Infections (viral & parasitic)
  • Dietary carcinogens
  • Chronic inflammation
Endogenous factors
  • Genetic
  • Hormones (promoters)
  • Immunity
44

Levels of cancer prophylaxis

Use: Prophylaxis stratified by the patient's baseline risk state, plus the tools used.

Levels
  • Primary — in an otherwise healthy person
  • Secondary — those who have premalignant conditions
  • Tertiary — avoiding second tumours in those cured of their original disease
Tools for prophylaxis
  • Avoid — environmental pollution, harmful lifestyles
  • Chemoprevention — tamoxifen (breast), nicotinamide/vit B3 (non-melanotic skin cancer), 13-cis-retinoic acid (reverse leukoplakia)
  • Risk-reduction surgery — breast (mastectomy), gastrectomy, thyroidectomy, colectomy
45

Cancer risk assessment & screening (prophylaxis)

Use: Prophylaxis has two approaches — risk assessment and screening. Risk assessment stratifies who needs prophylaxis across four axes. (Note: this lecture names screening as a prophylaxis tool but does not enumerate formal screening criteria.)

Genetic
  • Family history
  • Hereditary cancer syndromes
Diseases
  • Inflammatory bowel disease
  • Hepatitis B and C
Environmental
  • Physical or chemical carcinogens
Lifestyle
  • Smoking
  • Alcohol
  • Diet
  • Exercise
46

Chemotherapy setting classification

Use: When chemotherapy is given relative to surgery.

  • Primary — chemotherapy alone, no additional therapy; e.g. haematological malignancies (leukaemia, lymphoma)
  • Adjuvant — after curative surgery when high risk of relapse; e.g. node-positive breast cancer
  • Neoadjuvant — before surgery to downsize the tumour → less radical operation / clear resection margin
47

Radiotherapy setting & route classification

Use: When (setting) and how (route) radiotherapy is delivered.

Settings
  • Primary — alone; preferred over surgery in laryngeal, oropharyngeal cancer & facial BCC (organ/tissue preservation); e.g. seminoma, localized Hodgkin disease
  • Adjuvant — after breast lumpectomy to reduce local recurrence; cisplatin & 5-fluorouracil act as radiosensitizers
  • Neoadjuvant — downsize before surgery, e.g. rectal adenocarcinoma
Routes
  • Systemic — oral radioactive iodine
  • Teletherapy — external beam radiotherapy
  • Brachytherapy — source near/within the target tissue (cervical, breast, prostate)
48

Immunotherapy classification

Use: Active vs passive immune approaches in cancer.

Active
  • Non-specific — BCG in superficial bladder cancer
  • Specific — vaccines derived from tumour cells or antigen-presenting cells
Passive
  • Cytokines — interferon alpha activates natural killer cells and dendritic cells
49

Tumour marker categories & uses

Use: Substances produced by the tumour or by the body's response to it.

Three categories
  • Proteins — enzymes, hormones, or oncofoetal antigens
  • Genetic mutations
  • Epigenetic changes
Four uses
  • Diagnosis
  • Staging
  • Response to treatment
  • Tumour recurrence
50

Gompertzian tumour-growth model & doubling milestones

Use: Mathematical model of tumour growth with the key doubling figures.

Growth model
  • Early growth is exponential, then the growth rate slows
  • Slowing arises from difficulties with nutrition & oxygenation; tumour cells compete with host tissue and with each other
  • Best mathematical model = 'Gompertzian', not exponential
Doubling milestones
  • ≈45 doublings for a single cell to reach a 1 cm tumour (clinically occult → clinically manifest)
  • A further 15 doublings → a 1 kg tumour (≈1 billion cells), likely to be fatal
  • Faster cell cycle → shorter doubling time → more rapid disease → shorter expected survival

External Herniae

7 entries
51

Classification of external abdominal hernias

Use: Core framework for grouping every external abdominal hernia

Two major groups
  • Groin
  • Ventral
Groin
  • Inguinal — direct & indirect
  • Femoral
Ventral
  • Exits through the midline aponeurotic zone (linea alba)
52

Myopectineal orifice

Use: Single groin zone of weakness — origin of ALL groin hernias

  • Most important anatomic feature of the groin
  • All groin hernias originate from this single zone of weakness — covered only by transversalis fascia + peritoneum
  • Bisected by the inguinal ligament → inguinal canal (superiorly) + femoral canal (inferiorly)
Borders
  • Inferior: superior pubic ramus + pectineal (Cooper's) ligament
  • Medial: rectus abdominis + inguinal falx (conjoined tendon)
  • Superior: conjoined tendon (fusion of internal oblique + transversalis fascia)
  • Lateral: iliopsoas muscle + lateral border of the femoral sheath
53

Hesselbach's (inguinal) triangle

Use: Distinguishes direct from indirect inguinal hernia

Boundaries
  • Lateral border of the rectus sheath
  • Inferior epigastric vessels
  • Inguinal ligament
Hernia relations
  • Direct hernias occur through it — medial to the inferior epigastric arteries
  • Indirect hernias are lateral to it (and to the lateral umbilical ligaments, which contain the epigastric arteries)
54

Triangle of doom

Use: Laparoscopic no-tack zone — iliac vessels

Boundaries
  • Medially: vas deferens
  • Laterally: gonadal vessels
  • Inferiorly: peritoneal edge
Contents / risk
  • Contains the external iliac artery and vein
  • No tacks — risk of iliac-vessel injury
55

Triangle of pain

Use: Laparoscopic no-tack zone — nerves

Boundaries
  • Gonadal vessels medially
  • Iliopubic tract laterally
  • Peritoneal edge inferiorly
Contents / risk
  • Lateral femoral cutaneous nerve
  • Femoral branch of the genitofemoral nerve
  • Femoral nerve
  • Tacks → nerve entrapment → pain on the anterolateral thigh
56

Circle of death (corona mortis)

Use: Laparoscopic no-tack zone — profuse bleeding

  • Vascular ring: anastomosis of an aberrant artery from the external iliac artery with the obturator artery (from the internal iliac artery)
  • Avoid tacks — profuse bleeding if the ring is injured
57

Inguinal ligament vs iliopubic tract

Use: Anterior (open) vs posterior (laparoscopic) repair landmark

Inguinal (Poupart's) ligament
  • Inferior edge of the external oblique aponeurosis, ASIS → pubic tubercle
  • Turns posteriorly to form the 'shelving edge' — secures the inferior border of the mesh in OPEN (anterior) repair
  • Anterior-lamina structure — not seen in laparoscopic (posterior) repair
Iliopubic tract
  • Continuation of the transversus abdominis aponeurosis/fascia
  • Posterior to the inguinal ligament; pubic tubercle medially → over the femoral vessels → ASIS laterally
  • Posterior-lamina landmark in laparoscopic repair
  • Lateral to the internal ring, no tacks below it (risk to lateral femoral cutaneous, genitofemoral, femoral nerves)

Analgesia & Pain

6 entries
58

Types of Pain classification

Use: Classify pain by onset, mechanism + site

Acute
  • Superficial, somatic, visceral
Chronic
  • Persisting >3 months
  • Impacts on quality of life
Cancer
  • Caused by infiltration, obstruction, inflammation, treatment
Neuropathic
  • Lesion or dysfunction of nervous system
  • Shooting, burning, numbness
Dichotomies
  • Nociceptive vs neuropathic
  • Somatic vs visceral
59

Four-phase pain pathway framework

Use: Map any analgesic to where it acts on the pathway

  • Transduction -> transmission -> perception -> modulation
60

Opioid receptor & agonist classification

Use: Predict opioid efficacy + ceiling from binding class

Receptors
  • Mu / delta / kappa
  • Located in CNS, some in PNS
Agonism classes
  • Full agonist - bind with high efficacy
  • Partial agonist - bind with low efficacy
  • Mixed agonist/antagonist - bind with low efficacy
  • Antagonist - no efficacy, displaces drug
61

Simplified Opioid Conversion Chart / ratios

Use: Convert between opioids + routes

  • 24h PO morphine -> fentanyl: divide by 4
  • PO morphine -> SC diamorphine: divide by 3
  • PO morphine -> SC morphine: divide by 2
  • PO morphine -> PO oxycodone: divide by 2
  • PO oxycodone -> SC oxycodone: divide by 2
  • PO tramadol -> PO morphine: divide by 5
62

Multimodal pharmacological targets framework

Use: Choose drugs acting at different sites for balanced analgesia

Peripheral
  • Local anaesthetics, anticonvulsants, TCAs, opioids, anti-inflammatories
Central
  • Anticonvulsants, opioids, tricyclic/SNRI antidepressants, alpha-2 agonist (clonidine), LA
Descending
  • Anticonvulsants, opioids, tricyclic/SNRI, alpha-2 agonist
63

Acute pain treatment methods tree

Use: Structured menu of acute-pain treatment options

Remove cause of pain
  • Surgery, splinting
Drug treatment
  • Non-opioid drugs
  • Opioid drugs
Regional analgesia
  • High-tech: epidural infusion, LA with or without opioid
  • Low-tech: nerve blocks
Physical methods
  • Manipulation, TENS, acupuncture
Psychological methods
  • Relaxation, psychoprophylaxis, hypnosis

Postoperative Complications

5 entries
64

Precipitants of Postoperative MI — HATE SPORT

Use: Mnemonic for the precipitants of post-op myocardial infarction

  • H = Hypothermia
  • A = Anaemia
  • T = Tachycardia
  • E = Endotracheal tube
  • S = Shivering
  • P = Pain
  • O = Oxygenation deficiency
  • R = REM sleep rebound
  • T = Thrombophilia (clotting tendency)
65

Arrhythmia Management Algorithm

Use: Bedside triage of a post-op arrhythmia

Unconscious
  • CPR & consider defibrillation
Conscious + low BP
  • Fast HR → ?SVT/VT → DC cardioversion
  • Slow HR → speed up the heart
Conscious + normal/raised BP
  • Narrow complexes → ?SVT
  • Broad complexes → ?VT
66

BP = CO × SVR — Causes of Postoperative Hypotension

Use: Classify causes of post-op hypotension via BP = CO × SVR

Underlying pump dysfunction
  • IHD, valvular, cardiomyopathy, congenital, arrhythmia
Acquired pump dysfunction
  • Hypoxia, low Hb, abnormal pH, deranged K, hypo/hypercapnia, hypothermia, hypoglycaemia
Low circuit pressure
  • Sepsis, anaphylaxis, vasodilators
Inadequate pump filling
  • Hypovolaemia, haemorrhage, tamponade, pneumothorax, PE
67

Classification of Postoperative Haemorrhage (timing)

Use: Time-based classification of post-op haemorrhage

  • Primary — intraoperative
  • Reactive — within 24 hours (ligature slipping or missed vessel due to intraoperative hypotension)
  • Secondary — 7 to 10 days (vessel erosion from infection)
68

Predisposing Factors for Postoperative Complications (5-category framework)

Use: Framework for the predisposing factors to post-op complications

1. General patient condition
  • Extremes of age; comorbidities e.g. diabetes, obstructive jaundice; nutrition (obese/malnourished); immunosuppression (long-term steroids, post-chemo); pre-op MRSA colonisation
2. Surgical factors
  • Grade (minor/intermediate/major) & experience; duration; nature & extent; emergency; surgical start 21:00-07:00 = increased morbidity
3. Anaesthetic factors
  • Grade & experience; regional vs GA; agents used
4. Medical co-morbidities
  • Cardiovascular, respiratory (exercise tolerance), metabolic, haematological, cerebrovascular, renal, hepatic, neuromuscular, musculoskeletal
5. Drug therapy
  • Anticoagulants, steroids, MAOIs, antiplatelets

Trauma (ATLS)

4 entries
69

LEMON airway-difficulty assessment

Use: Assess for a difficult airway before intubation in trauma.

LEMON
  • Look externally
  • Evaluate — 3-3-2 rule
  • Mallampati
  • Obstruction
  • Neck mobility
3-3-2 rule
  • 3 fingers in the mouth
  • 3 fingers from mentum to hyoid
  • 2 fingers from floor of mouth to thyroid cartilage
70

Trauma airway management escalation ladder

Use: Stepwise airway management in trauma.

  • Open — jaw thrust
  • Clear — suction
  • Maintain — OPA or NPA
  • Oxygenate — high-flow O2
  • Ventilate — BVM (if needed)
  • Secure — SGD/LMA → ETT via RSI → surgical cricothyroidotomy (FONA)
  • Monitor — SpO2, ETCO2
71

Six immediately life-threatening thoracic conditions (Breathing)

Use: Exclude and treat these in the Breathing (B) step of the primary survey.

  • Laryngo-tracheal injury
  • Tension pneumothorax
  • Open chest wound
  • Flail chest
  • Massive haemothorax
  • Cardiac tamponade (flagged SBA)
  • Traumatic cardiac arrest flagged alongside as a reversible cause to exclude
72

ATMIST / ATMISTE trauma handover

Use: Structured trauma handover from the prehospital team (ATMIST) / prehospital ED alert (ATMISTE).

ATMIST (handover)
  • Age
  • Timings
  • Mechanism of injury
  • Injuries
  • Signs & symptoms
  • Treatment
ATMISTE (prehospital alert — adds)
  • Sex / relevant history
  • Estimated Time of Arrival