Emergency medicine Flashcards

Question

Describe the prescribing for breakthrough pain

Answer 1

Immediate release morphine – 1/6th to 1/10th of regular 24 hour dose, as required up to a maximum of 6 doses in 24 hours If 3 or more doses given within 4 hours review, if more than 6 doses in 24 hours review

Answer 2

Divide weak opioid dose by 10 to get morphine dose

Answer 3

Oral morphine to SC morphine – divide by 2 Oral morphine to SC diamorphine – divide by 3 Oral morphine to oral oxycodone – divide by 4 Oral morphine to SC hydromorphone – divide by 10

Answer 4

Triggers – rapid dose escalation, renal impairment, sepsis, electrolyte abnormalities, drug interactions Symptoms: Persistent sedation Vivid dreams, hallucination, shadows at edge of visual field Delirium Muscle twitching/myoclonus/jerking Abnormal skin sensitivity to touch

Answer 5

Pre-renal: Hypovolaemia – haemorrhage, over-diuresis, vomiting, diarrhoea Renal artery stenosis Low effective arterial blood volume – heart failure, cirrhosis, sepsis, third-spacing Drug-induced – NSAIDs, ACE inhibitors, diuretics Intra-renal: Acute tubular necrosis – most common cause of AKI due to ischaemic or toxic injury to cells of PCT Acute interstitial nephritis – drug-induced, infection, immune-mediated Glomerular disease – primary renal disease, systemic disease with or without immune complex deposition Intra-tubular obstruction – multiple myeloma with paraprotein, pigment Other – scleroderma renal crisis, malignant hypertension Post-renal (obstructive): Ureters – nephrolithiasis, retroperitoneal fibrosis Bladder – bladder cancer Prostate – benign prostate hyperplasia, prostate cancer Urethra – urethral stricture External – retroperitoneal mass, ovarian tumours

Answer 6

GFR alteration: ACE inhibitors ARBs Cyclosporin NSAIDs Tacrolimus Tubular cell toxicity: Aminoglycosides Amphotericin B Cisplatin Interstitial nephritis: NSAIDs Rifampicin Crystal nephropathy: Acyclovir Ampicillin

Answer 7

AKI if any of the following present: Urine output <0.5ml/kg/hour for 6 hours Serum creatinine increased by 1.5x baseline over 7 days Serum creatinine increase by 0.3mg/dL in 48 hours AKI stages I – rise in creatinine of 1.5-1.9x baseline, <0.5ml/kg/hour urine output for 6 hours II – rise in creatinine of 2-2.9x baseline <0.5mg/kg/hour urine output for 12 hours III – rise in creatinine of >3x baseline <0.3ml/kg/hour for 24 hours

Answer 8

Older age Diabetes Chronic kidney disease Chronic liver disease Congestive cardiac failure Polypharmacy Hypotension Hypovolaemia Drugs – ACEi, ARBs, NSAIDs, contrast

Answer 9

General management: Withdrawal of nephrotoxic medication Adjustment of drug doses which are renally cleared to prevent toxicity Fluid resuscitation Urinary catheterisation – measure urine output, relieve urinary obstruction Assess for evidence of sepsis and initiate sepsis six bundle if required Targeted management dependent on cause Renal replacement therapy – indications: Metabolic acidosis pH less than 7.15 or worsening acidaemia Refractory electrolyte abnormalities (hyperkalaemia over 6.5mmol) Presence of dialysable toxins – toxic alcohols, aspirin, lithium Refractory fluid overload – diuretics resistant fluid overload with AKI End-organ uraemic complications e.g. pericarditis, encephalopathy, uraemic bleeding

Answer 10

Fluid overload Electrolytes derangement – hyperphosphataemia, hyperkalaemia Acid-base disorder – metabolic acidosis End-organ complications of uraemia Chronic kidney disease End-stage renal disease Death

Answer 11

Purposeful (e.g. fights – usually hands, sexual violence) or incidental (sports, occupational injury) Most common bacterial agents – strep spp, staph aureus, haemophilus spp., eikenella corrodens, bacteroides spp., other anaerobes Also small risk of transmission of viruses such as HIV and herpes simplex Infections common, especially in clenched fist injuries (‘fight bites’)

Answer 12

Dogs Puncture and ripping/tearing/shearing wounds – make contact and hold on, powerful jaws which can cause significant tissue injury including crush wounds, devascularisation, bone damage, soft-tissue avulsion Generally polymicrobial, most common bacterial agents – S aureus, pasteurella canis, P. multocida, capnocytophaga canimorsus (rare but serious) Also risk of rabies (most commonly from dogs) – very low risk in the UK, more likely to be from bats Cats Fine sharp teeth – narrow, deep puncture wounds inoculated with saliva, able to penetrate bone, joints and tendons 2x as likely as dog bites to become infected due to deep inoculation, and deep infections such as abscesses and osteomyelitis more common as only small opening for drainage Generally polymicrobial – pasteurella multocida common, can cause severe, rapidly-spreading infections

Answer 13

Immediate wound management: Remove foreign bodies e.g. teeth Encourage wound to bleed Irrigate thoroughly with saline (1L) Provide analgesia Consider antibiotics if indicated – human bite which has broken skin and drawn blood, or high-risk area (hands, feet, face, genitals), risk factors for infection or clinical signs of infection (co-amoxiclav) If visibly infected send pus or deep wound swab for culture (before cleaning wound) Consider tetanus booster Consider need for debridement – keep fasted ?Close wound ?Referral for assessment by plastics team Assessment: Document how bite occurred, whether skin was broken, and blood drawn Examine bite – location, size and depth, type of wound, degree of crush injury, devitalised tissue, nerve/tendon damage, involvement of muscle/bone/joints/vessels Check ROM if over a joint Neurovascular function distal to bite – pulses and sensation Signs of infection Facial – intraoral examination to exclude cheek lacerations with intraoral communication ?X-ray – fractures or foreign bodies Assess BBV risk Consider possible child protection issues or safeguarding issues for vulnerable adult

Answer 14

Over 24 hours old Infected Deep puncture wounds Crush injuries Heavy contamination Uncertain adequacy of debridement Bites to limbs, hands and feet

Answer 15

Cause - borrelia burgdorferi, spirochete bacteria spread by ticks Early features (within 30 days) Erythema migrans – ‘bulls-eye’ rash at site of tick bite Typically develops 1-4 weeks after initial bite Usually painless, >5cm in size and slowly increases Systemic – headache, lethargy, fever, arthralgia Late features (after 30 days) Cardiovascular – heart block, peri/myocarditis Neurological – facial nerve palsy, radicular pain, meningitis Management Early disease – doxycycline Disseminated disease - ceftriaxone

Answer 16

Usually from source in rectum or colon, can also be due to upper GI bleed Diverticular disease Ischaemic or infective colitis Haemorrhoids Malignancy Angiodysplasia Crohn’s disease Ulcerative colitis Radiation proctitis

Answer 17

Usually from source in rectum or colon, can also be due to upper GI bleed Diverticular disease Ischaemic or infective colitis Haemorrhoids Malignancy Angiodysplasia Crohn’s disease Ulcerative colitis Radiation proctitis

Answer 18

A-E assessment, resuscitation Major haemorrhage protocol Hb <70 (or <80 and cardiovascular disease) require transfusion Reverse anti-coagulation If unstable – CT angiogram to identify bleeding point, can then stop bleeding with IR (arterial embolisation) or endoscopic haemostasis (adrenaline injection, electrocoagulation, clips or bands) May need surgical intervention If stable – elective colonoscopy

Answer 19

Oesophageal causes Varices – large volume fresh blood Oesophagitis – small volume fresh blood, often streaking vomit, preceded by GORD symptoms Cancer – small volume except as preterminal event with erosion of major vessels Mallory-Weiss tear – small to moderate volume bright red blood following repeated vomiting Gastric causes Ulcer – small volume unless erosion into significant vessel, tends to present as IDA Cancer – frank haematemesis or altered blood mixed with vomit, dyspepsia, constitutional symptoms Dieulafoy lesion – developmental AV malformation, causes large haemorrhage Diffuse erosive gastritis – haematemesis, epigastric pain Duodenal causes Ulcer – haematemesis, melena, epigastric discomfort Aorto-enteric fistula – following previous abdominal aortic aneurysm surgery, major haemorrhage with high mortality

Answer 20

Haematemesis – frank or ‘coffee ground’ Melaena – tar-like, black, offensive stools (altered blood) Haematochezia – fresh blood PR if large volume upper GI bleed Symptoms of underlying cause - abdominal pain (epigastric), jaundice, ascites Haemodynamic instability – hypotension, tachycardia, pre-syncope, other signs of shock

Answer 21

Risk assessment: Glasgow-Blatchford score on first assessment Rockall score after endoscopy Resuscitation: A to E assessment IV access – ideally two wide bore cannulae Bloods – FBC, U&Es (acute rise in urea with GI bleed), coagulation screen, LFTs (cirrhosis), crossmatch IV fluid resuscitation, transfusion Platelets given to those actively bleeding with platelet count <50 FFP if actively bleeding and PT or APTT >1.5x normal Fibrinogen <1.5g/L despite FFP give cryoprecipitate Prothrombin complex if taking warfarin and actively bleeding Terlipressin – suspected variceal bleeding Prophylactic antibiotic therapy – suspected or confirmed variceal bleeding (ciprofloxacin) Endoscopy for all unstable patients with severe UGIB immediately after resuscitation (within 24 hours for all others) Endoscopic haemostatic techniques: Peptic ulcer - adrenaline injection, cauterisation Varices – banding, Sengstaken-Blakemore tube if severe/uncontrollable bleeding PPI can be used in variceal bleeding pre-endoscopy to reduced risk of re-bleed – NICE advise against PPI pre-endoscopy

Answer 22

Glasgow-Blatchford score Pre-endoscopy, on initial assessment Identifies low-risk patients who don’t need intervention Components – urea, haemoglobin, SBP, pulse >100, melaena, syncope, hepatic disease, cardiac failure Rockall score Can be done pre- or post-endoscopy, post is more accurate Identify risk of ongoing bleeding and death Components – age, shock, comorbidities (cardiac failure, ischaemic heart disease, renal failure, liver failure, malignancy), diagnosis, major Major stigmata of recent haemorrhage on endoscopy – dark spot, blood in upper GI tract, adherent clot, visible or spurting vessel

Answer 23

Signs of airway compromise – stridor, hoarse voice, tachycardia, hypoxia, cyanosis Singed nasal hairs Facial burns Soot deposits around nose Requires early involvement of anaesthetics for potential intubation

Answer 24

By mechanism: Thermal burns – scalds, flame injuries, contact burns Electrical burns – low-voltage, high-voltage Chemical burns – acids, alkalis By depth: Superficial epidermal (previously 1st degree) – red, painful, dry, no blisters Partial thickness (superficial dermal, previously 2nd degree) – pale pink, painful, blistered, slow CRT Partial thickness (deep dermal, previously 2nd degree) – typically white, can have patches of non-blanching erythema, reduced sensation, painful to deep pressure Full thickness (previously 3rd degree) – white/brown/black, no blisters, no pain By percentage total body surface area (%TBSA) – various techniques for estimate, e.g. Wallace’s rule of nines, the ‘rule of palm’ (palm area is 1% of total body surface area, only accurate up to 15%) or Lund and Browder chart (most accurate, mainly paediatric)

Answer 25

Complex All electrical and chemical burns Any burn affecting a critical area – face, hands, feet, perineum or genitalia, crossing joints, circumferential Any thermal burn covering >15% TBSA in adults, >10% in children (>5% in children under 1) Non-complex Partial thickness thermal burn covering up to 15% TBSA in adults, up to 10% in children (up to 5% in children under 1) that does not affect a critical area Deep partial thickness burns covering up to 1% of the body

Answer 26

Remove any source of burns and non-adherent clothing A-E assessment: Airway – signs of inhalation injury, consider intubation Breathing – 100% oxygen via non-rebreather mask, evaluate need for escharotomy if circumferential burns, do ABG and check carboxyhaemoglobin levels for carbon monoxide poisoning Circulation – two wide bore IV cannula, routine bloods, aggressive IVF, insert urinary catheter for fluid balance monitoring Disability – evaluate neurological status, check temperature as risk of hypothermia Exposure – fully expose patient to get accurate estimation of %TBSA burned and check for concomitant injuries IV morphine for analgesia Strict fluid balance chart Clingfilm for initial wound dressing to minimise fluid loss Reduce risk of hypothermia – warmed room, warmed fluids, reduce wound exposure time Give tetanus booster if needed

Answer 27

First-aid Remove source of burn and any non-adherent clothing Wound under running water for 20 minutes as soon as possible Clean with normal saline Analgesia Emollients Leave blisters intact Non-adherent dressing

Answer 28

Fluids calculated from time of burn If clinically shocked on arrival, correct this before calculating burn fluid requirements Modified Parkland formula most commonly used – describes the volume of crystalloid fluid to be administered in the first 24 hours post-burn: Initial 24 hours (adult) = 4ml x weight (kg) x %TBSA Initial 24 hours (children) = 3ml x weight (kg) x %TBSA 50% volume given in first 8 hours, remaining 50% in next 16 hours Known to underestimate requirements in large full-thickness burns, inhalation injury and electrical burns Maintain urine output >0.5ml/kg/hour

Answer 29

All 2% or more TBSA in children or 3% or more in adults All deep partial or full-thickness burns All circumferential Any chemical, electrical or friction burns or cold injuries Any burn not healed in two weeks Suspicion of NAI Burns over perineum, face, hands, feet, genitals, major joints Pregnant or severe co-morbidities

Answer 30

Superficial and superficial partial thickness usually heal naturally in three weeks, conservative management Burn unit or burn centre care for more severe burns Wound debridement – excision of necrotic tissue, may need amputation if unsalvageable limbs Grafting – autograft (from patient’s body), allograft (from another human donor) or xenograft (from another species, typically pig) Prognosis: Superficial – heals without scarring Superficial partial-thickness – heals without scarring Deep partial thickness – heals in 3-8 weeks, likely to scar if taking >3 weeks to heal Full thickness – heals by contracture, >8 weeks, will scar

Answer 31

Typically in >25% TBSA, >65 years old or <2 years old, those with simultaneous major trauma or smoke inhalation Systemic inflammatory response where exaggerated and dysregulated inflammatory response develops due to large burn injury, may progress to multiple organ dysfunction syndrome, where inflammatory response causes end-organ failure Inflammatory response causes fluid third-spacing Immunosuppression, bacterial translocation from gut lumen

Answer 32

Early: Respiratory distress from smoke inhalation (causes bronchospasm, pulmonary and laryngeal oedema) or circumferential chest burn Poising from inhalation of noxious gases Fluid loss, hypotension, hypovolaemic shock Hypothermia Wound infection and sepsis Toxic shock syndrome – small burns in children, infected with staph aureus Cardiac arrhythmias – electrical burns (ventricular fibrillation), electrolyte disturbance Vascular insufficiency, distal ischaemia, compartment syndrome from circumferential burn of limb/digit AKI – hypovolaemia, muscle breakdown (rhabdomyolysis), haemolysis Limb loss Curling’s ulcer – ischaemia of gastric mucosa, can cause GI bleeding or perforation Death Late: Wound infection AKI – sepsis, multi-organ failure, nephrotoxic drugs Chronic neuropathic pain/itch Contractures Scarring Psychosocial impact Sleep disorders

Answer 33

Cardiac causes: Acute coronary syndrome – central crushing chest pain, radiates to left arm and/or jaw, lasting longer than 20 minutes, associated sweating, nausea, SOB Stable angina – sudden onset chest pain radiating to left arm and/or jaw lasting for less than 20 minutes, triggered by exertion, complete resolution during rest Pericarditis – gradual onset central chest pain worse lying flat, better leaning forwards Thoracic aortic dissection – sudden onset central chest pain radiating to back, ‘tearing’ nature Respiratory causes: Pneumonia – gradual onset sharp chest pain, pleuritic, associated productive cough, SOB, fever Spontaneous pneumothorax – sudden onset sharp pleuritic chest pain, SOB Pulmonary embolism – sudden onset pleuritic chest pain, SOB, haemoptysis GI causes: GORD – central chest pain, burning, worse lying flat, associated nausea/vomiting Oesophageal spasm – central chest pain, associated dysphagia, heartburn, regurgitation Boerhaave’s syndrome – sudden onset severe chest pain after severe vomiting MSK causes: Costochondritis Muscle strain Chest wall trauma Psychosocial/psychological causes: Anxiety Functional pain

Answer 34

Plasma potassium 5.5mmol/L or more Mild – 5.5-5.9 Moderate – 6.0-6.4 Severe >6.5

Answer 35

Renal: AKI CKD Hyperkalaemic renal tubular acidosis Iatrogenic: ACEi/ARBs Potassium-sparing diuretics e.g. spironolactone NSAIDs Digoxin (toxicity) Trimethoprim Beta-blockers Heparin Ciclosporin Tacrolimus Other: Trauma and burns DKA – extracellular Addison’s disease Pseudohyperkalaemia – blood sample inaccurate

Answer 36

General weakness and fatigue Palpitations, chest pain, SOB Usually no clinical signs Bradycardia – due to AV block Depressed or absent tendon reflexes

Answer 37

Tall, tented T waves Wide QRS Prolonged PR Flattened/absent P AV block Bradycardia

Answer 38

If potassium less than 6, stable renal function, no ECG changes – no urgent treatment, stop precipitants Potassium >6 with ECG changes or >6.5 – urgent treatment Prevent further accumulation of potassium: Stop IV fluids containing potassium Suspend medications which could increase potassium Suspend supplements containing potassium Stabilise cardiac membrane: IV calcium gluconate if ECG changes (reduces risk of fatal arrhythmia for 30-60 minutes), repeat if ECG changes not improving Shift potassium intracellularly: Insulin-glucose infusion Salbutamol Remove potassium from body: Calcium resonium Correct underlying cause Haemodialysis if refractory hyperkalaemia

Answer 39

Potentially life-threatening cardiac arrhythmias Muscle weakness Paralysis

Answer 40

Hypokalaemia with alkalosis Vomiting Thiazide and loop diuretics Cushing’s syndrome Conn’s syndrome (primary hyperaldosteronism) Hypokalaemia with acidosis Diarrhoea Renal tubular acidosis Acetazolamide Partially treated DKA Magnesium deficiency – can be difficult to normalise until magnesium deficiency corrected

Answer 41

Muscle weakness Hypotonia Muscle cramps Severe – flaccid paralysis, hyporeflexia

Answer 42

U waves Small or absent T waves Prolonged PR ST depression

Answer 43

U waves Small or absent T waves Prolonged PR ST depression

Answer 44

Mild, able to eat and drink – oral supplements (e.g. SandoK) Moderate to severe, ongoing losses, unable to take oral – IV replacement IV potassium given at maximum rate of 10mmol/hour on a ward 40mmol/1L 0.9% NaCl Remember to check Mg and replace if deficient Treat underlying cause

Answer 45

Serum sodium <135

Answer 46

Classified in terms of extracellular fluid status and urine sodium concentration Urinary sodium >20mmol/L Hypovolaemic – diuretics (thiazide, loop), Addison’s, diuretic renal failure Euvolaemic – SIADH, hypothyroidism Hypervolaemic – acute tubular necrosis Urinary sodium <20mmol/L Hypovolaemic – vomiting or diarrhoea, sweating, burns Euvolaemic – acute fluid overload Hypervolaemic – congestive cardiac failure, liver cirrhosis, nephrotic syndrome, psychogenic polydipsia

Answer 47

Mostly asymptomatic Usually related to volume status e.g. overloaded and oedematous or clinically dehydrated Severe hyponatraemia – neurological signs including malaise, headache, confusion, progressing to reduced consciousness and seizures

Answer 48

Need to know - Is it acute or chronic? Acute - less than 48 hours Chronic - more than 48 hours Severity of hyponatraemia Mild – 130-134 Moderate – 120-129 Severe - <120 Symptoms – is the patient symptomatic? Suspected aetiology Hypovolaemic Euvolaemic Hypervolaemic Management: Consider precipitating medications and stop Chronic hyponatraemia Hypovolaemic cause – normal isotonic saline Euvolaemic/hypervolaemic cause – fluid restrict Acute hyponatraemia with severe symptoms Close monitoring – HDU or above Hypertonic saline (3% NaCl) to correct sodium more quickly

Answer 49

Rapid correction can cause central pontine myelinolysis – change in extracellular osmolality causes damage to myelin sheaths of brainstem neurons Present with confusion and balance problems, develop pseudobulbar palsy and quadriplegia

Answer 50

Complication of treatment – osmotic demyelination syndrome (central pontine myelinolysis) Cellular swelling – cerebral oedema (raised ICP), impaired healing of tissues post-op ECG changes – non-ischaemic ST elevation

Answer 51

Sodium >145 Symptoms usually only seen if >160

Answer 52

Hypovolaemic Diuretics – loop mainly Dehydration/fluid restriction – diarrhoea, vomiting, burns, febrile illness Acute tubular necrosis Hyperosmolar states – including HHS Euvolaemic – diabetes insipidus Hypervolaemic Excessive hypertonic saline administration Steroid excess – Conn’s syndrome or Cushing’s syndrome

Answer 53

Generally asymptomatic Excessive thirst Severe – weakness, lethargy, irritability, confusion, seizures, coma >180 – ataxia, tremor, coma, seizures

Answer 54

Urine osmolality – hypernatraemia stimulates ADH release from hypothalamus, concentrates urine to reabsorb more water If urine osmolality >600mOsmol/kg – hypothalamic and renal function intact, extra-renal cause If urine osmolality <600mOsmol/kg with hypernatraemia, indicates ADH or renal-dependent mechanism, such as osmotic diuresis or diabetes insipidus

Answer 55

Replace fluid deficit and correct serum sodium relatively slowly (risk of cerebral oedema) Rate of no more than 0.5mmol/hour correction, or 10mmol/L/day in chronic hypernatraemia Enteral fluid replacement preferred, including via NG if needed If unable to tolerate enteral replacement use 5% dextrose (most preferred), 0.9% saline (if volume depleted) or Hartmann’s

Answer 56

Malignant: PTHrp production – squamous cell carcinoma Bone primary tumours or metastases – osteolysis Myeloma – increased osteoclastic bone resorption Primary hyperparathyroidism - most common Sarcoidosis Thiazide diuretics Acromegaly Thyrotoxicosis Dehydration Addison’s disease Paget’s disease of bone – prolonged immobilisation

Answer 57

Malignant PTHrp production – squamous cell carcinoma Bone primary tumours or metastases – osteolysis Myeloma – increased osteoclastic bone resorption Primary hyperparathyroidism Sarcoidosis Thiazide diuretics Acromegaly Thyrotoxicosis Dehydration Addison’s disease Paget’s disease of bone – prolonged immobilisation

Answer 58

Rehydration with normal saline – 3-4L/day May use bisphosphonates after rehydration Other options – calcitonin (quicker than bisphosphonates), steroids in sarcoidosis

Answer 59

Vitamin D deficiency Chronic kidney disease Hypoparathyroidism e.g. post-thyroid/parathyroid surgery Pseudohypoparathyroidism – target cells insensitive to PTH Rhabdomyolysis Magnesium deficiency – end-organ PTH resistance Massive blood transfusion Acute pancreatitis

Answer 60

Tetany – muscle twitching, cramping, spasm Perioral paraesthesia Chronic – depression, cataracts ECG – prolonged QT Trousseau’s sign – carpal spasm if brachial artery occluded with BP cuff Chvostek’s sign – tapping over parotid causes facial muscles to twitch

Answer 61

Severe (tetany, seizures, prolonged QT) – IV calcium replacement, calcium gluconate, with ECG monitoring Further management depending on underlying cause

Answer 62

Drugs – diuretics, PPIs TPN Diarrhoea Alcohol Hypokalaemia Hypercalcaemia – secondary to hyperparathyroidism, compete for reabsorption in loop of Henle Metabolic disorders – Gitleman’s and Bartter’s

Answer 63

Paraesthesia Tetany Seizures Arrhythmias Decreased PTH secretion – hypocalcaemia ECG similar to hypokalaemia

Answer 64

Severe (tetany, arrhythmias, seizures) – IV magnesium replacement Mild – oral magnesium salts (can cause diarrhoea)

Answer 65

Haemolysis CKD Magnesium toxicity – pre-eclampsia management Mild hypermagnesemia – DKA, adrenal insufficiency, hypothyroidism, hyperparathyroidism, lithium toxicity

Answer 66

Weakness Confusion Hyporeflexia Arrhythmias Hypotension Respiratory depression

Answer 67

Mild and normal kidney function – no treatment except stopping drugs which may precipitate Severe – calcium gluconate, calcium chloride IV loop diuretics

Answer 68

Evidence of damage to the brain as a result of trauma to the head, represented by reduced GCS or focal neurological deficit Mild traumatic brain injury – concussion, transient disturbance in the function of the brain caused by head injury Focal e.g. contusion/haematoma Extradural, subdural or intracranial haematoma Contusions – coup or contre-coup Diffuse e.g. diffuse axonal injury Occurs due to mechanical shearing of axons following deceleration Secondary brain injury due to physiological response to head injury – cerebral oedema, ischaemia, herniation

Answer 69

Describes the relationship between the contents of the skull and intracranial pressure – skull is a closed rigid box with fixed capacity Volume of brain is made up of – brain tissue, CSF, blood If volume of one of these increases, to maintain a constant ICP, the volume of one of the others must decrease Initially this can be achieved through compliance – mechanisms to keep intracranial pressure constant (e.g. decrease blood or CSF volume with space-occupying lesion) Eventually compensatory mechanisms are exhausted and intracranial pressure begins to rise, eventually leading to herniation of brain tissue Uncal herniation – displacement of medial part of temporal lobe (uncus) below tentorium cerebelli Tonsillar herniation – cerebellar tonsils forced down through foramen magnum, causing compression on the brainstem

Answer 70

Headache – worse in morning, worse with Valsalva manoeuvres, worse lying down Nausea and vomiting Visual disturbance Reduced GCS Slow, slurred speech Papilloedema Ipsilateral sluggish dilated pupil  fixed dilated pupil Cranial nerve palsy Seizures Abnormal respiration Abnormal posturing – decorticate then decerebrate Cushing’s triad – physiological response to raised ICP, aims to improve perfusion Bradycardia Hypertension Irregular breathing

Answer 71

CPP = mean arterial pressure – intracranial pressure (rise in ICP reduces CPP)

Answer 72

Hypoxia and hypercapnia – maintain sats 94-98%, intubate to protect airway if poor respiratory effort Hypovolaemia and hypotension – resuscitate with IV fluids or blood products, vasopressors Cerebral oedema and raised ICP – position at 30 degrees to aid venous drainage, mannitol or hypertonic saline to reduce ICP, intubation and hyperventilation strategies Expanding haematoma – reverse coagulation abnormalities, consider transexamic acid if <3 hours post-injury, neurosurgical intervention (craniectomy, Burr holes) Hypoglycaemia or hyperglycaemia – maintain normal glucose with insulin/dextrose Increased metabolic demand e.g. hyperthermia or seizures – maintain normothermia, anti-convulsants if seizure activity

Answer 73

Cervical spine immobilisation if required A-E assessment A - GCS <8 cannot protect own airway, anaesthetic support required, avoid head-tilt chin-lift and nasopharyngeal airways B – oxygen to prevent hypoxia C – fluid resuscitation D – GCS recorded and repeated every 30-60 minutes, pupil assessment, BM (avoid hypoglycaemia) E – examine for lacerations, facial fractures, depressed skull fractures, basal skull fractures

Answer 74

Within 1 hour: GCS <13 on initial assessment GCS <15 2 hours after injury Suspected open or depressed skull fracture Any sign of basal skull fracture – haemotympanum, panda eyes, CSF leakage, Battle’s sign Post-traumatic seizure Focal neurological deficit More than 1 episode of vomiting Within 8 hours: Age >65 History of bleeding or clotting disorders, on anticoagulant therapy Dangerous mechanism of injury – pedestrian or cyclist hit by car, fall from height greater than 1m or 5 steps More than 30 minutes retrograde amnesia of events before injury

Answer 75

Within 1 hour, one of: Suspicion of NAI Traumatic seizure without history of epilepsy At 2 hours after injury, GCS less than 15 Suspected open or depressed skull fracture or tense fontanelle Sign of basal skull fracture Focal neurological deficit If under 1, bruising, swelling or laceration >5cm on head Within 1 hour if more than one of: Loss of consciousness >5 mins Abnormal drowsiness Three or more discrete episodes of vomiting Dangerous mechanism of injury Amnesia lasting more than 5 minutes

Answer 76

Loss of consciousness at time of injury then prolonged post-traumatic coma without expected neurological recovery MRI best for detection (often missed on CT) Limited options for treatment – prevent secondary brain injury, close monitoring including of ICP, rehabilitation Spectrum of clinical consequences, most severe is long-term vegetative state

Answer 77

Collection of blood between the dura and skull Typical aetiology – traumatic injury, particularly to pterion (point of union of frontal, parietal, temporal, and sphenoid bones), which causes bleeding from middle meningeal artery (branch of maxillary from external carotid) Can also occur with venous bleeding Presentation: Headache Nausea and vomiting Confusion Loss of consciousness – immediately after head injury, followed by period of lucidity, then progressively decreasing level of consciousness several hours later Signs – reduced GCS, focal neurological deficits, hyperreflexia, spasticity, Babinski’s sign, Cushing’s triad

Answer 78

‘Lemon-sign’ – dura attached to sutures, blood trapped and creates hyperdense biconvex bulge as cannot expand past sutures, can cause mid-line shift and herniation

Answer 79

Correction of coagulation abnormalities – reverse anticoagulants ?Anticonvulsants ?Reduce ICP – mannitol, barbiturates Definitive management Conservative management if small with minimal midline shift Burr hole craniotomy to allow evacuation of haematoma Trauma craniotomy – acute EDH with significant mass effect Generally good prognosis if early evacuation of haematoma Complications: Infection – skull fracture or post-op Seizures Cognitive impairment Hemiparesis Hydrocephalus Brainstem injury – significantly raised ICP

Answer 80

Correction of coagulation abnormalities – reverse anticoagulants ?Anticonvulsants ?Reduce ICP – mannitol, barbiturates Definitive management Conservative management if small with minimal midline shift Burr hole craniotomy to allow evacuation of haematoma Trauma craniotomy – acute EDH with significant mass effect Generally good prognosis if early evacuation of haematoma Complications: Infection – skull fracture or post-op Seizures Cognitive impairment Hemiparesis Hydrocephalus Brainstem injury – significantly raised ICP

Answer 81

Collection of blood between dura and arachnoid mater Acute – present <3 days following injury Subacute – present 3-21 days after injury Chronic – present >21 days after injury Occur secondary to high or low energy trauma Low-energy trauma more common in elderly, alcoholics – shrinkage of brain, fragile brains Due to shearing of bridging veins – usually venous bleeding, often deceleration injury Presentation: Acute – loss of consciousness, headache, focal neurology, signs of raised ICP Chronic – progressive worsening confusion, memory loss, ataxia

Answer 82

‘Banana sign’, crescent shaped, blood free to flow around brain between dura and arachnoid Can cause midline shift, less than extra-dural Acute – hyperdense as fresh blood Chronic – hypodense altered blood

Answer 83

Non-contrast CT head

Answer 84

Correct coagulation abnormalities – reverse anticoagulation ?Anticonvulsants Definitive Conservative – small bleed with minimal mass effect Trauma craniotomy – acute SDH with significant mass effect Large bleed/lots of cerebral oedema – hemicraniectomy Burr hole craniotomy – chronic SDH, allows evacuation of blood Complications: Permanent neurological deficits Coma Seizures Infection Recurrent subdural haematoma

Answer 85

Decreased level of consciousness Nausea/vomiting Constipation Pruritus Confusion Respiratory depression Miosis

Answer 86

A-E assessment A/B – may need airway adjuncts/intubation due to decrease consciousness/respiratory depression Remove source if possible – e.g. transdermal patch, syringe driver Close monitoring – potential to deteriorate rapidly Naloxone – competitive opioid receptor antagonist IV, IM, SC, intranasal (most commonly IV acutely) Almost instant response but short-lived (half-life 60-90 minutes), initial improvement with recurrence of opiate overdose features if further doses not given Risk in IV drug users that they will abscond then relapse into coma when naloxone wears off Chonic pain or palliative care patients – risk of causing distress/pain if fully reverse opioids, give small doses of naloxone and titrate to effect High dose opioids – naloxone infusion better than intermittent boluses Can precipitate acute withdrawal syndrome and nausea and vomiting

Answer 87

Respiratory depression --> death Acute lung injury after heroin overdose is common – presents with symptoms acute respiratory distress syndrome

Answer 88

Re-uptake inhibition – increased action of serotonin (5-HT receptors) and noradrenaline Post-synaptic receptor antagonism – decreased action of histamine (H1 receptors), A-1 adrenoreceptors, acetylcholine receptors Also act on fast sodium channels in myocardial cells – sodium channel blockade

Answer 89

Symptoms within six hours of ingestion Anticholinergic toxicity – dry mouth, blurred vision, confusion, constipation, tachycardia, urinary retention Noradrenaline – tachycardia, tremor Sodium channel blockade – palpitations, arrhythmias Serotonin - hyperthermia Can presents with reduced consciousness, seizures ECG – widened QRS, prolonged QTc Predispose to ventricular tachycardia and ventricular fibrillation ABG - mixed acidosis Hypokalaemia

Answer 90

No specific management – supportive Oxygen Continuous monitoring with ECG Fluid bolus if hypotensive Benzodiazepines for seizures Activated charcoal if present within one hour of ingestion – prevents absorption Sodium bicarbonate in arrhythmia and acidosis to prevent progression to ventricular arrhythmias Cooling measures for hyperpyrexia Catheterise if urinary retention

Answer 91

Causes mixed respiratory alkalosis and metabolic acidosis – stimulation of respiratory centre causes hyperventilation and respiratory alkalosis, direct effects of salicylates combined with acute renal failure may lead to metabolic acidosis Features: Hyperventilation Tinnitus - ototoxicity Lethargy Sweating, pyrexia Nausea/vomiting Hyper/hypoglycaemia Confusion Seizures Coma

Answer 92

ECG – monitor for arrhythmias, QRS widening and QT prolongation BM – hypoglycaemia/hyperglycaemia ABG – monitor acid-base balance, initially respiratory alkalosis then metabolic acidosis Plasma salicylate concentration – taken >2 hours after ingestion, repeat 2 hourly until peak Mild less than 300mg/L Moderate 300-700mg/L Severe >700mg/L U&Es – hypokalaemia common Coagulation – INR and PT may be increased in hepatic dysfunction

Answer 93

A-E assessment Protect airway Supportive care, consider ICU admission Activated charcoal if within 1 hour of ingestion of >125mg/kg IV fluid Potassium replacement – must do before bicarbonate Sodium bicarbonate – enhances urinary excretion, alkalinises urine Ongoing management: Cooling Haemodialysis – if renal failure, severe metabolic acidosis, seizures, salicylate concentration >900mg/L or >700 with acidosis or coma Benzodiazepines for seizures

Answer 94

Seizures Acute respiratory distress syndrome Coma Arrhythmia – cardiac arrest Drug-induced hepatitis

Answer 95

CV – hypotension, bradycardia, AV block, heart block Respiratory – bronchospasm Metabolic – hypoglycaemia, hyperkalaemia Neurological – coma, seizures

Answer 96

Resuscitation – fluids Hypoglycaemia – dextrose Hyperkalaemia management Activated charcoal if <1 since ingestion Consider atropine if bradycardic In resistant cases may use glucagon

Answer 97

Ingested total overdose in >1 hour

Answer 98

Increased risk of hepatotoxicity: Taking liver enzyme-inducing drugs – rifampicin, phenytoin, carbamazepine, chronic alcohol excess, St John’s wort Malnourish e.g. anorexia, haven’t eaten in a few days Acute alcohol intake is not associated with increased risk, may be protective

Answer 99

Early symptoms: Nausea and vomiting Abdominal pain If massive overdose can develop acidosis and coma early Signs of hepatotoxicity (1-5 days post-ingestion): RUQ pain Jaundice Renal failure Transaminitis Coagulation abnormalities Hypoglycaemia Hepatic encephalopathy Multi-organ failure Death

Answer 100

Need further assessment if – self-harm, symptomatic, taken 75mg/kg or more in within an hour, 75mg/kg or more in any 24-hour period and more than licensed dose in 24 hours, more than licensed dose in 24 hours and taken any paracetamol products in preceding 2 or more days If non-staggered overdose presenting within 24 hours of ingestion May benefit from activated charcoal if within 1 hour of overdose – rare Take bloods at least 4 hours after ingestion (U&Es, HCO3, LFTs, FBC, INR, glucose, paracetamol level) Ingested <150mg/kg – wait for results of bloods, plot on nomogram Ingested over 150mg/kg –if won’t have blood results within 8 hours from ingestion then start NAC If above treatment line on nomogram start NAC (if started and below treatment line can stop), give two NAC infusions Can stop NAC when INR <1.3, ALT <100 and ALT <2x admission and paracetamol <20 If non-staggered after 24 hours Take bloods If features of hepatotoxicity start NAC, if none NAC not required If staggered Start NAC Take bloods Assess for hepatotoxicity - if none can stop NAC

Answer 101

Arterial pH less than 7.3, 24 hours after ingestion Or all of the following: PT more than 100 Creatinine >300 Grade III/IV encephalopathy

Answer 102

Enhance GABA resulting in sedative, anxiolytic, anticonvulsant and muscle relaxant effects Features: Reduced consciousness Respiratory depression Hypotension Bradycardia Rhabdomyolysis Hypothermia

Answer 103

A-E assessment Airway may be compromised by reduced consciousness – manoeuvre, adjuncts, anaesthetics involvement Oxygen Wide-bore IV cannulae, bloods (including CK) ECG – may have arrhythmias IV fluids – hypotension Flumazenil – GABA receptor antagonist Reverses CNS depression caused by benzodiazepines Only used if requiring ventilation, only benzodiazepines (no possibility of mixed OD), patient is not benzodiazepine dependent Risks of seizures if used incorrectly

Answer 104

Dehydration Hyponatraemia Renal failure Drugs – diuretics (thiazides), ACEi/ARB, NSAIDs, metronidazole

Answer 105

Coarse tremor Hyperreflexia Acute confusion Polyuria Seizure Coma

Answer 106

Mild-moderate – IVF ?Sodium bicarb – urine alkalisation to promote excretion Haemodialysis for severe toxicity

Answer 107

0.4-1.0mmol/L >1.5 - usually toxicity

Answer 108

Desferrioxamine – chelating agent

Answer 109

Carbon monoxide binds readily to haemoglobin forming carboxyhaemoglobin – reduced oxygen-carrying capacity Oxygen saturation of haemoglobin decreases – early plateau in oxygen dissociation curve

Answer 110

Headache – most common Nausea and vomiting Vertigo Confusion Subjective weakness Severe toxicity – pink skin, hyperpyrexia, arrhythmias, extrapyramidal features, coma

Answer 111

Pulse oximetry may be falsely high – similarity between oxyhaemoglobin and carboxyhaemoglobin VBG/ABG should be done Management: 100% high-flow oxygen, for minimum 6 hours Hyperbaric oxygen?

Answer 112

Measure serum lead level - >10 is significant FBC – microcytic anaemia Blood film – red cell abnormalities, basophilic stippling, clover-leaf morphology Management: Chelating agents – Dimercaptosuccinic acid D-penicillamine EDTA Dimercaprol

Answer 113

Abdominal pain Peripheral neuropathy – mostly motor Neuropsychiatric features Fatigue Constipation Blue lines on gum margin

Answer 114

Hydroxycobalamin

Answer 115

Anti-histamines e.g. cyclizine, promethazine Dopamine antagonists, act by blocking the chemoreceptor trigger zone – prochlorperazine (used for chemotherapy-induced N+V), chlorpromazine hydrochloride, haloperidol (used in palliative care), domperidone (used in Parkinson’s, less likely to cause central effects) 5HT3-receptor antagonists – ondansetron (for N+V in those receiving cytotoxics) Dexamethasone (for chemotherapy induced N+V), mechanism not fully understood Metoclopramide – inhibit D2 and 5-HT3 receptors in chemoreceptor trigger zone

Answer 116

Primary – purpose is to rapidly identify and manage impending or actual life threats to patient C – catastrophic haemorrhage A – airway with C-spine control B – breathing C – circulation D – disability E - exposure Secondary – after primary survey completed, immediate life-threats identified and managed and patient is stable Continue to monitor A-E Examine head to toe for injuries, including log roll to look at back Can include FAST scan – focused assessment with sonography for trauma Look for intraperitoneal free fluid

Answer 117

Eyes Open spontaneously – 4 Open to voice – 3 Open to pain – 2 No response – 1 Motor Obeys commands – 6 Localises to pain – 5 Normal flexion/withdrawal to pain – 4 Abnormal flexion (decorticate posturing) – 3 Abnormal extension (decerebrate posturing) – 2 None – 1 Voice Speech orientated to time, person, place – 5 Confused speech – 4 Inappropriate words – 3 Incomprehensible sounds – 2 None – 1

Answer 118

Adult - 30 compressions, 2 breaths Child - 15 compressions, 2 breaths

Emergency medicine Flashcards

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