Clinical Medicine Emergencies PDF

752 Lumbar puncture (LP) Contraindications Bleeding diathesis. Cardiorespiratory compromise. Infection at site of needle insertion. Most importantly: ICP (suspect if very severe head- ache, ...

752 Lumbar puncture (LP) Contraindications Bleeding diathesis. Cardiorespiratory compromise. Infection at site of needle insertion. Most importantly: ICP (suspect if very severe head- ache, level of consciousness with falling pulse, rising BP, vomiting, focal neurology, or papilloedema)—LP in these patients will cause coning, so unless it is a routine pro- cedure, eg for known idiopathic intracranial hypertension, obtain a CT prior to LP. CT is 18 Practical procedures not infallible, so be sure your indication for LP is strong. Method Explain to the patient what sampling CSF entails, why it is needed, that co- operation is vital, and that they can communicate with you at all stages. Place the patient on their left side, with the back on the edge of the bed, fully flexed (knees to chin). A pillow under the head and another between the knees may keep them more stable. Landmarks: plane of iliac crests through the level of L3/4 (fig 18.8). In adults, the spinal cord ends at the L1/2 disc (fig 18.9). Mark L3/4 intervertebral space (or one space below, L4/5), eg by a gentle indentation of a needle cap on the overlying skin (better than a ballpoint pen mark, which might be erased by the sterilizing fluid). Use aseptic technique (mask, gloves, gown) and 2% chlorhexidine in 70% alcohol to clean the skin, allow to dry, and then place sterile drapes. Open the spinal pack. Assemble the manometer and 3-way tap. Have three plain sterile tubes and one fluoride tube (for glucose) ready. Using a 25G (orange) needle, raise a bleb of local anaesthetic, then use a 21G (green) needle to infiltrate deeper. Wait 1min, then insert spinal needle (22G, stilette in place) perpendicular to the body, through your mark, aiming slightly up towards the umbilicus. Feel resist- ance of spinal ligaments, and then the dura, then a ‘give’ as the needle enters the subarachnoid space. NB: keep the bevel of the needle facing up, parallel with dural fibres. Withdraw stilette. Check CSF fills needle and attach manometer (3-way tap turned off towards you) to measure ‘opening’ pressure. Catch fluid in numbered bottles (to volume required, mark tubes in advance). Remove needle and apply dressing. Document the procedure clearly in the notes including CSF appearance and opening pressure (in cmH2O). Send CSF promptly for microscopy, culture, protein, lactate, and glucose (do plasma glucose too)—call the lab to let them know. If applicable, also send for: cy- tology, fungal studies, TB culture, virology (± herpes and other PCR), syphilis ser- ology, oligoclonal bands (+ serum sample for comparison) if multiple sclerosis suspected. Is there xanthochromia (p474)? If you fail; ask for help—try with the patient sitting (but opening pressure is unre- liable) or with radiological guidance. CSF composition Normal values Lymphocytes 40% is life-threatening. Early haem- atocrit and FBC may be misleading after major acute blood loss: transfuse based on clinical criteria and observations. Until blood group is known, use group O red cells. Females 3600m). Differential diagnosis Asthma/COPD, pneumonia. May coexist. Symptoms Dyspnoea, orthopnoea (paroxysmal), pink frothy sputum. Symptoms of precipi- tant: MI, infection. Signs HR, RR, pink frothy sputum, pulsus alternans, JVP, fine lung crackles, triple/gallop rhythm (p42), wheeze. If significant hypoxia: sitting up, leaning forward, distressed, pale, sweaty. Also signs of cause/precipitants. Investigations CXR (p135, p706–8): cardiomegaly, bilateral airspace shadowing, effusions (check costophrenic angles), fluid in lung fissures, Kerley B lines (septal linear opacities). ECG: ischaemic changes/MI, tachycardia, arrhythmia. U&E (AKI), troponin (raised in ACS), ABG (hypoxia, raised lactate in cardiogenic shock). BNP/NT-proBNP (p135): useful −ve predictive value if BNP 12. Moderate CSF protein, lymphocytes (table 19.4, p807), glu- cose often normal. Viral PCR including HSV (high sensitivity and specificity, though may be negative early in disease course so consider repeat). Do not delay treat- ment if encephalitis is suspected and LP is delayed. CSF will remain PCR positive for a few days so can be done after treatment is given. Bloods HIV, blood culture, serum for viral PCR, throat swab, toxoplasma IgM titre, malaria film. Consider autoantibody testing. MRI Abnormal in 90% of HSV encephalitis. Normal or subtle abnormalities in auto- immune encephalitis. CT, CT-PET If paraneoplastic cause suspected. EEG Diffuse abnormalities are non-specific and can be abnormal in encephalopathy due to other causes. Management Mortality in untreated viral encephalitis is >70%. Aciclovir 10mg/kg/8h IV for 14d. Consider repeat CSF HSV PCR at 14 days to con- firm discontinuation. May need longer (eg 21d) if immunosuppressed. Supportive therapy in high-dependency unit or critical care may be needed. Monitor kidney function with IV aciclovir (small risk of crystal nephropathy). CMV encephalitis: ganciclovir, foscarnet. Toxoplasmosis: see p421. Symptomatic treatment: eg anticonvulsant medication for seizures (p810).  Cerebral abscess 809 Suspect in any patient with ICP and signs of infection, eg fever, WCC. Can occur in the absence of systemic signs of inflammation especially if immunosuppressed. Consider risk: Recent ear, sinus, dental, or periodontal infection. Skull fracture. Congenital heart disease, endocarditis. 19 Emergencies Bronchiectasis. Immunosuppression. Signs Fever. Focal neurological signs. Seizure. Signs of ICP: papilloedema, seizures, focal neurology, reduced conscious level. Signs of infection elsewhere, eg teeth, ears, lungs, endocarditis. Investigations WCC, ESR, blood culture, HIV, CT/MRI (see p730), drainage and culture. Treatment Urgent neurosurgical referral for evacuation. Treat ICP (p814). Antimicrobial therapy depends on likely source, (eg Streptococcus milleri or oro- pharyngeal anaerobes from frontal sinuses or teeth, Bacteroides fragilis or anaer- obes from ear), immunosuppression (risk of toxoplasmosis), and local sensitivities. Seek expert advice from microbiology/infectious disease physicians. 810 Status epilepticus Definition Clinical or electroencephalographic (EEG) seizure activity for 5 minutes or more, or recurrent seizures without recovery in between. (The historical defin- ition of seizure activity for >30min is not practical or appropriate given the urgent need for treatment.) Usually occurs in patients with known epilepsy. Diagnosis of tonic–clonic status is usually clear. Non-convulsive status (eg absence or continuous partial seizures with preserved consciousness) may be more difficult: look for subtle eye or lid movement. For other signs, see p480, pp486–9. An EEG can be very helpful. 19 Emergencies Could the patient be pregnant? If so, manage as eclampsia (occurs after 20 weeks’ gestation so a pelvic mass is palpable): obstetric help, IV magnesium, and delivery when stable (OHCS p90). Investigations Capillary glucose. Other tests after treatment: FBC, U&E, Ca2+, ABG, ECG. MRI (if first presentation of seizure). Consider: anticonvulsant concentrations, toxicology screen, LP, blood and urine culture, EEG, carbon monoxide concentration. Management See fig 19.24.9 Basic life support. Treat hypoglycaemia. If the patient has an individualized emergency management plan that is immedi- ately available, administer medication as detailed in the plan. If no individualized emergency management plan: 1 Benzodiazepine IV lorazepam: 4mg, repeat after 5–10min. Use if no delay to IV access and re- suscitation facilities available. Beware respiratory depression. Buccal midazolam: 10mg, repeat after 5–10min. Rectal diazepam: 10–20mg, repeat after 5–10min. 2 Second-line IV anticonvulsant If ongoing seizure activity.Follow local guid- ance. For example: Levetiracetam: 60mg/kg (max 4500mg) IV over 10min. Can use in patients al- ready on levetiracetam. Avoid if known advanced CKD. Phenytoin: 20mg/kg (max 2000mg) IV at max rate of 50mg/min. ECG and blood pressure monitoring due to risk of hypotension and bradycardia. Use with cau- tion in elderly and in cardiac disease (consider rate, eg ≤25mg/min). Sodium valproate: 40mg/kg (max 3000mg) IV over 10min. Avoid in pregnancy, advanced liver disease, mitochondrial disease. Continue medication given as a loading dose as a maintenance treatment ac- cording to expert neurology advice. Give maintenance dose of levetiracetam or sodium valproate 12h after loading, or phenytoin 6–8h after loading. 3 Refer to critical care for general anaesthesia if above measures fail. Adjuncts: Dexamethasone 10mg IV if vasculitis/cerebral oedema (tumour) possible. IV thiamine in malnutrition/alcohol withdrawal. What was the cause? Consider precipitants, eg hypoglycaemia, pregnancy, alcohol, drugs, CNS lesion or infection, hypertensive encephalopathy, inadequate anticonvulsant dose, non-adherence (p486). Consider non-epileptic seizures (p460) if atypical features: pelvic thrusts, re- sisting eye-lid opening or passive movements, flailing rather than clonic move- ments of limbs.  811 19 Emergencies Fig 19.24 Management of status epilepticus. 812 Head injury Initial management See fig 19.25.10 Do not presume GCS is due to intoxication unless a head injury has been excluded. Stabilize airway, breathing, and circulation. If GCS ≤8 seek anaesthetic or critical care expertise in order to protect the airway. If GCS ≤12 without active extracranial bleeding, give tranexamic acid 2g IV. Involve neurosurgeons early if GCS, falling GCS, persistent confusion, ICP sus- pected, abnormal intracranial imaging, CSF leak, penetrating injury. Monitor HR, BP, T°, RR, pupil size/symmetry every 15min. 19 Emergencies Complete neurological examination is needed. Assess amnesia. Distinguish antero- grade (from time of injury, post-traumatic) and retrograde (events prior to injury). There is no risk to cervical spine if low-risk features: rear-end motor collision, com- fortable sitting, ambulatory, no cervical spine tenderness, delayed-onset pain, and able to actively rotate neck 45° to the left and right. Nurse semi-prone if no spinal injury. CT head Within 1h if: GCS ≤12 on initial assessment, or GCS 1m or 5 stairs. Retrograde amnesia (events before head injury) of >30min. CT cervical spine Within 1h if any of the following: GCS ≤12 on initial assessment. The patient has been intubated. Definitive diagnosis of cervical spine injury is needed urgently (eg before surgery). The patient is having other body areas scanned, eg due to polytrauma. Clinical suspicion of cervical spine injury and increased risk due to any of: Age ≥65yrs. High-impact injury. Focal neurological deficit or limb paraesthesia. Unsafe to assess the range of movement in the neck. Person cannot actively rotate neck 45° to left and right in safe assessment. Condition predisposing to higher risk of injury, eg axial spondyloarthritis. MRI cervical spine If neurological signs or symptoms of cervical spine injury or if needed to clarify CT findings. MRA if suspicion of vascular injury. Admission and observation New, clinically important abnormalities on CT (consider anticoagulant treatment in assessing significance). GCS has not recovered to pre-injury baseline. Ongoing symptoms, eg persistent vomiting, seizures, severe headache, meningism. Other injuries or safe-guarding concerns. Complications Extradural/subdural haemorrhage (p476), seizures (pp810–11), hypo- pituitarism (p819), Parkinsonism, dementia. Poor prognostic indicators: decerebrate rigidity, extensor spasms, prolonged coma, BP, PaO2, T° >39°C.  813 19 Emergencies Fig 19.25 Immediate management of head injury. 814 Raised intracranial pressure (ICP) The volume inside the cranium is fixed, so any increase in the contents can lead to raised ICP. This can be mass effect, oedema, or obstruction to fluid outflow. ICP leads to secondary brain injury and death, so needs urgent treatment. Normal ICP in adults is 20mmHg suggests ICP. Causes Primary or metastatic tumours. Head injury (pp812–13). Haemorrhage: subdural, extradural, subarachnoid, intracerebral, intraventricular. 19 Emergencies Infection: meningitis (pp806–7), encephalitis (p808), brain abscess (p809). Hydrocephalus. Cerebral oedema. Status epilepticus (pp810–11). Idiopathic. Signs and symptoms History of trauma. Headache (worse on coughing, leaning forwards), vomiting. Altered GCS: drowsiness, listlessness, irritability, coma. HR and BP (Cushing’s response). Irregular/Cheyne–Stokes respiration. Pupil changes: constriction first, later dilation (do not mask these signs by using agents such as tropicamide to dilate the pupil for fundoscopy). Visual acuity, peripheral visual field loss. Papilloedema has low sensitivity for ICP. Loss of venous pulsation at the optic disc is more sensitive but difficult to detect and may be absent in ~10% of population. Investigations U&E, FBC, LFT, glucose, serum osmolality, clotting, blood culture. Consider toxicology screen. CXR, and other source of infection that might indicate abscess. CT head. LP if papilloedema with normal imaging: measure the opening pressure. Management See fig 19.26. The goal is to ICP and avert secondary injury. Urgent neurosurgery may be required for definitive treatment of ICP from focal causes. This can be achieved via evacuation, or temporized with burr hole/craniotomy. An ICP monitor (or bolt) can be placed to monitor pressure and guide neurosurgical critical care. Herniation syndromes Uncal herniation A supratentorial mass pushes the inferomedial temporal lobe (uncus) through the tentorial notch (the opening between supratentorial and infratentorial regions of the brain), to compress the midbrain. The IIIrd nerve, travelling in this space, gets compressed, causing a dilated ipsilateral pupil, then ophthalmoplegia (a fixed pupil does not localize the lesion: it is due to compression, not the lesion itself, but does indicate the side of the lesion). This may be followed (quickly) by contralateral hemiparesis due to pressure on the cerebral peduncle. Coma then occurs due to pressure on the ascending reticular activating system in the midbrain. Cerebellar tonsil herniation Pressure in the posterior fossa forces the cerebellar tonsils through the foramen magnum. Ataxia, VIth nerve palsy, and up-going plantar reflexes occur first, then loss of consciousness, irregular breathing, and apnoea. May proceed very rapidly given the small size and poor compliance of the posterior fossa. Subfalcian (cingulate) herniation A frontal mass forces the cingulate gyrus (medial frontal lobe) under the rigid falx cerebri. May be silent unless the anterior cerebral artery is compressed and causes a stroke: contralateral leg weakness ± abulia (lack of decision-making).  815 19 Emergencies Fig 19.26 Immediate management of raised intracranial pressure. 816 Diabetic ketoacidosis (DKA) Mechanism Insulin deficiency and an increase in counter-regulatory hormones (glucagon, catecholamines, cortisol) lead to metabolism of triglycerides and amino acids in- stead of glucose for energy. Overproduction of -hydroxybutyric acid, acetoacetic acid, and acetone ('fruity' breath) leads to acidosis. Early recognition and treatment are important. The combination of acidosis and hyperglycaemia can be fatal. Presentation 19 Emergencies Unexplained weight loss, vomiting, abdominal pain, polyuria, polydipsia, lethargy, anorexia, dehydration, rapid/deep breathing (= ‘Kussmaul’ hyperventilation, con- sider if RR without hypoxia), drowsiness, coma. Check glucose in all patients with diabetes who are unwell. Triggers for DKA in- clude infection, surgery, MI, pancreatitis, medication (eg corticosteroids, calcineurin inhibitors, thiazides, antipsychotics, SGLT2 inhibitors (see BOX)), wrong insulin dose/ non-adherence. Diagnosis 1 Acidaemia (pH 6mmol/L. GCS 40). 3 Consider surgical management if severely reduced visual acuity, severe and persistent/deteriorating visual field defects, or GCS. 4 Other pituitary hormone replacement only after established on glucocorticoid. 5 Close monitoring of pituitary and visual function by specialist endocrine/neuro- surgical service. 820 Phaeochromocytoma emergency Rare, life-threatening emergency due to release of high concentrations of cate- cholamines. Mimics other conditions, therefore difficult to diagnose if not known to have a phaeochromocytoma/paraganglioma. Occurs spontaneously, or may be a triggering event: trauma, surgery, medication, eg corticosteroids, -blockers (un- opposed -blockade can  effects), metoclopramide, anaesthetic agents. Signs and symptoms Emergency = symptoms of phaeochromocytoma (severe hypertension, headache, sweating/fever, anxiety, palpitations) plus life-threatening complications: 19 Emergencies Haemodynamic instability: labile SBP 60–250mmHg. End-organ dysfunction: cardiac (LVF, IHD, arrhythmia cardiogenic shock), pul- monary (oedema, ARDS), neurological (encephalopathy, stroke, seizure), renal (AKI), hepatic (acute liver failure), GI (paralytic ileus, intestinal ischaemia), metabolic (lactic acidosis, DKA, rhabdomyolysis), coagulopathy. Investigation Plasma metanephrines (metanephrine, normetanephrine, 3-meth- oxytyramine), CT (adrenal), MRI (extra-adrenal), functional scan, eg PET-CT, genetics. Management Aims: medical stabilization and sufficient -blockade to block cat- echolamine effects. Get help from critical care and endocrinology. -blockade Titrate to BP control, eg: Doxazosin 4–32mg/d PO (selective, tachycardia). Phenoxybenzamine 10mg/12h PO, up to 1mg/kg/d (non-selective, tachycardia). Phentolamine 2–5mg IV. Short acting. Repeat if required. -blocker Only after -blockade if tachycardia, arrhythmia, myocardial ischaemia. Volume Expansion if required. Supportive care As well as management of end-organ dysfunction. Surgery For resectable disease once stable with sufficient -blockade and appro- priate volume expansion. Thyroid emergencies Hyperthyroid crisis ('thyrotoxic storm') Signs and symptoms T°, agitation, confusion, tremor, tachycardia, AF/arrhythmia, heart failure, D&V, acute abdomen (exclude surgical causes), proptosis/exophthalmos/ ophthalmoplegia, goitre, thyroid bruit, coma. Triggers: infection, surgery. Investigation TSH, free T4, free T3, TSH-receptor antibodies (+ve in Graves’ dis- ease). Also: U&E, FBC, LFT, calcium, glucose, ECG. Look for precipitants: CXR, blood and urine cultures. Treatment See fig 19.28. Seek endocrinology advice. Myxoedema coma Signs and symptoms Hypothyroid appearance (p215, fig 5.16), hypothermia, brady- cardia, hypercapnic respiratory failure, hyporeflexia, hypoglycaemia, psychosis ('myxoedema madness'), seizure, coma. Triggers: infection, MI, stroke, trauma. Investigation TSH, free T4, free T3, U&E (often Na+). Also cortisol, glucose, FBC, ABG, infection screen: CXR, blood and urine cultures. Treatment Seek endocrinology advice. Secure airway, O2 if hypoxic. Refer to critical care. Correct hypoglycaemia: eg 100mL 20% glucose IV over 15min. Assume (relative) cortisol deficiency until tests prove otherwise: hydrocortisone 100mg IV (p821). Thyroid hormone replacement, eg liothyronine (T3) 5–10mcg PO/NG (risk of car- diac complications if IV), repeat/titrate depending on response/cardiac status. Thyroxine (T4) can also be used but conversion to T3 may be  in severe illness. Dose depends on cardiac risk, eg 25–75mcg/day PO/NG. IV fluids if needed for volume depletion: care due to risk of pulmonary oedema. Other: slow warming, treat infection. Establish on oral thyroxine before discharge.  821 19 Emergencies Fig 19.28 Management of hyperthyroid crisis. 822 Acute poisoning The patient may or may not be able to tell you what they have taken. If there are any tablets with the patient use MIMS Colour Index, EMIMS images, BNF descrip- tions, or online drug identification services, eg TICTAC visual ID system. Examination and investigations May offer a clue as to the toxin taken: Fast/irregular pulse Salbutamol, tricyclic, quinine, phenothiazine (p827). Respiratory depression Opiate (p826), benzodiazepine (p826). Hypothermia Phenothiazine (p827), barbiturate. 19 Emergencies Hyperthermia Amphetamine, MAOIS, cocaine, ecstasy (p827). Coma Benzodiazepine (p826), alcohol, opiate, tricyclic, barbiturate. Seizures Hypoglycaemics, tricyclic, phenothiazine (p827), theophylline, cocaine. Constricted pupils Opiates (p826), organophosphate (p827). Dilated pupils Amphetamine, cocaine, quinine, tricyclics. Hyperglycaemia Organophosphates, theophylline, MAOIS. Hypoglycaemia Insulin, sulfonylurea, alcohol, salicylate (p825). Kidney injury Salicylate (p825), paracetamol (p824), ethylene glycol. Acidosis Salicylate (p825), carbon monoxide (p826), iron (p826), alcohol, ethylene glycol. Osmolality Alcohol, ethylene glycol (p660). Management 1 ABC: secure airway. O2 if hypoxic. 2 Blood: check paracetamol and salicylate concentrations. Other drug concentra- tions and assessment of toxicity guided by toxin taken (or likely toxin taken). 3 Reduce toxicity: activated charcoal (p823) and/or specific treatment (pp826–7). 4 Information: if in doubt how best to act, contact the National Poisons Information Service. Advice is available 24/7 via your NHS unit's login, the TOXBASE app, or UK phone information line: 0844 892 0111. 5 Supportive care: Monitor GCS and ensure safe airway. O2 if hypoxic. May need intubation, venti- lation, critical care. Monitor: according to toxin, T°, HR, BP, RR, O2 sats, glucose, ECG, urine output. Treat hypoglycaemia (p818). IV fluids if volume deplete. Cool/warm if hypo/hyperthermia. Psychiatric assessment Be kind. Aim to establish: Intentions at time. Was this a suicide attempt? If so, was the act planned? Did they take precautions against being found? Did the patient seek help after- wards? Does the patient think the method was dangerous? Any final act, eg suicide note? Present intentions. Do they still feel suicidal? What problems led to the act and do they still exist? Is there a psychiatric disorder? Is there an established diagnosis or current symptoms, eg depression, psychosis, schizophrenia, dementia, substance misuse disorder, personality disorder? What are the patient’s resources, eg friends, family, work, personality? Assess suicide risk See OHCS p726. There is risk of death in the first year following a presentation with attempted suicide. Risk factors for future suicide include: Intention to die. Social isolation. Psychiatric disorder. Unemployed. Poor resources. Male. Previous suicide attempts. >50yrs old. Refer for psychiatric assessment and support Seek advice about all presenta- tions with deliberate self-poisoning. Refer for formal assessment if symptoms or known to have a psychiatric disorder, or if high suicide risk. Toxicology Check blood glucose, paracetamol, and aspirin concentrations. 823 Necessity of other assays and tests depends on the drug taken, the anticipated toxicity, and the index of suspicion. Be guided by the National Poisons Information Service (p822). Therapeutic monitoring is available for some poisons, eg digoxin, methanol, lithium, anti-epileptic drugs, iron, theophylline. Screening of urine, especially for recreational drugs, may be useful in some, but not all, cases (see BOX ‘New psychoactive substances’). New psychoactive substances 19 Emergencies New ‘designer’ drugs, with chemical properties similar to established illicit drugs, may cause toxicity. They were termed 'legal highs' until UK legislation banned them in 2016. These drugs pose a difficult problem for the assessing physician as the precise chemistry and mechanisms of action of both the active compound, as well as any impurities, are often unclear. They can cause life-threatening compli- cations and death. Obtain as much detail as possible about specific agents taken in a drug history; there may be no available screening tool. Decontamination Do not induce vomiting. Activated charcoal Binds toxins in GI tract to  absorption. Includes: ACE-i, amphetamine, anti- depressants (not lithium), antiepileptics, aspirin, benzodiazepines, -blockers, calcium-channel blockers, digoxin, diuretics, oral hypoglycaemic drugs, opiates, paracetamol, death cap, ricin, yew, ie taxanes. The sooner activated charcoal is given, the more effective it is. It is generally effective up to 1h after ingestion, but longer if poisons are: Adsorbed beyond the stomach in the distal GI tract. Modified-release preparations. Slowly absorbed. Undergo significant enterohepatic or entero-enteric circulation which is inter- rupted by activated charcoal. (In entero-enteric circulation, the intestinal wall functions as a semipermeable membrane: toxins can diffuse out of the blood onto the charcoal in the intestinal lumen.) A multi-dose regimen is useful in poisoning due to carbamazepine, quinine, dap- sone, phenobarbital, theophylline, digoxin, slow-release quetiapine, aspirin, ami- triptyline, phenytoin, sotalol, oxcarbazepine, lamotrigine, citalopram, venlafaxine, eg 50g/4h (if unable to tolerate, reduce to 25g/2h or 12.5g/h though may  efficacy). Activated charcoal does not adsorb alcohols or metals so is ineffective in poi- soning due to lithium, lead, mercury, organic solvents, acids/bases, cyanide. Gastric lavage Rarely used as outcome studies (in high-income countries with access to sup- portive care and antidotes) do not show benefit. Risks include pulmonary aspiration, laryngospasm and hypoxia, perforation. Haemodialysis May be indicated if significant toxicity from substances that can be cleared by haemodialysis, eg alcohol, ethylene glycol, methanol, aspirin, lithium, barbiturates, sodium valproate, phenytoin, carbamazepine, theophylline. 824 Paracetamol poisoning 12g (= 24 tablets) or 150mg/kg in adults may be fatal. If >110kg, calculate ingested dose using a weight of 110kg to avoid underestimating toxicity. If the patient is malnourished then 75mg/kg can kill. Signs and symptoms None initially, or vomiting ± RUQ pain. Later, jaundice and encephalopathy from liver damage, AKI. Management Decontamination Activated charcoal 1g/kg (max 50g) if 8h after ingestion, before paracetamol concentration available. Stop later if concentration below line (use clinical judgement, review INR and ALT). Unknown timing or staggered overdose. Seek expert advice if HIV, enzyme-inducing drugs, alcohol, or nutrition affects in- terpretation of paracetamol nomogram, or in critical illness. Scottish and Newcastle Acetylcysteine Protocol (SNAP) regimen: 1 Bag 1: 100mg/kg NAC in 200mL 5% glucose/0.9% sodium chloride over 2 hours. 2 Bag 2: 200mg/kg NAC in 1000mL 5% glucose/0.9% sodium chloride over 10 hours. Send LFTS, INR, venous blood gases, paracetamol concentration at 10 hours (2 hours before end). If INR ≤1.3 and ALT normal and paracetamol level 4mmol/L: moderate toxicity. >500mg/kg ≈ blood salicylate concentration >6mmol/L: severe toxicity. Signs and symptoms Unlike paracetamol, there are many early features: Mild toxicity: tinnitus, tachypnoea, nausea, vomiting, headache, abdominal pain. Moderate toxicity: tachypnoea, tachycardia, orthostatic hypotension, confusion, slurred speech, hallucinations, hypoglycaemia. Severe toxicity: cerebral and pulmonary oedema, hypotension, arrhythmias. Hypoventilation heralds respiratory failure: prepare for intubation. Management 1 Activated charcoal 1g/kg (max 50g) to all presenting within 1h of ingestion. Consider repeat doses (two further doses of 50g, 4h apart) as food in the stomach, bezoar formation, and pyloric sphincter spasm due to aspirin can all delay absorption. 2 Investigations Paracetamol and salicylate concentrations, U&E, bicarbonate, lactate, ABG, glucose, FBC, clotting studies, calcium, magnesium, LFT. ECG and car- diac monitor. Repeat salicylate concentrations every 2h to assess for delayed absorption/increasing toxicity. 3 Fluid balance and urine output Correct volume and K+ depletion. Consider catheterization to monitor output and pH. 4 Alkalization of urine Enhances excretion. Consider if moderate toxicity/rising concentration, eg 1L 1.2–1.4% sodium bicarbonate IV over 3–4h. Aim for urine pH 7.5–8. NB: monitor serum K+ as hypokalaemia may occur, and should be re- placed, caution if AKI. 5 Haemodialysis For moderate and severe toxicity. Contact nephrology early. 6 Supportive care Correct hypoglycaemia (p818), treat seizures (pp810–11), early critical care input. 7 Psychiatric assessment Assess before discharge home. 826 Specific poisons and antidotes Anticoagulants See pp346–7. Benzodiazepines Symptoms Sedation, coma, respiratory depression. Treatment Supportive. Ensure airway. Ventilation and haemodynamic support may be needed. Risks of reversal with flumazenil outweigh benefits for most. Risk of provoking seizures, which are then treatment resistant. Use only after expert advice. -blocker 19 Emergencies Symptoms Bradycardia, hypotension. Treatment Atropine 500mcg IV, repeat up to 3mg (pp792–3). Glucagon, eg 5–10mg IV over 2min, then infusion of 50–150mcg/kg/h. Contact cardiology for temporary pacing. Evidence for calcium (eg 10mL of 10% calcium chloride), IV insulin plus dextrose, Intralipid®. Cyanide Binds iron and inhibits the cytochrome system. Leads to anaerobic respir- ation and lactic acidosis. Symptoms Mild: dizziness, anxiety, tachycardia, nausea, confusion. Moderate: reduced consciousness, convulsions, cyanosis, arrhythmias. Severe: coma, fixed pupils, cardiorespiratory failure, death. Treatment 100% O2. If mild, supportive care is usually sufficient. If moderate/ severe, specific treatment to bind cyanide is required, eg: Hydroxocobalamin (Cyanokit®) 5g over 15min, repeated once if required. Sodium thiosulfate: 50mL of 25% sodium thiosulfate (12.5g) IV over 10min. Repeat after 30–60min if required. Carbon monoxide Despite hypoxaemia, skin is pink or pale (not blue), as carb- oxyhaemoglobin (COHb) displaces O2 from Hb binding sites. For the same reason, O2 saturation measured by a pulse oximeter may be normal. Check ABG in a co- oximeter (ie ensure it measures haemoglobin, SaO2, Meth-Hb, and COHb): SaO2 and COHb (normal 50%): seizures, coma, cardiac arrest. Treatment Remove source. Give 100% O2 until COHb 25–30%, neurological features, cardiovascular impairment, failure to respond to treatment, pregnancy. Digoxin Symptoms GI upset, diarrhoea, yellow-green visual halos, palpitations, cognition. ECG ST 'scooping', ventricular ectopics, bidirectional VT (beat-to-beat alteration of QRS axis). Treatment Activated charcoal, correct K+. If severe/life-threatening toxicity, eg ventricular arrhythmia, high-grade heart block, or concentration >15ng/mL: in- activate with digoxin-specific antibody fragments (DigiFab®). Dose according to amount ingested, or use concentration and weight. Iron 60mg/kg causes severe toxicity and mortality. Symptoms GI upset, shock, metabolic acidosis, coagulopathy, cardiomyopathy, AKI, liver dysfunction/failure. Healing of bowel leaves scarring and stenoses. Treatment Desferrioxamine 15mg/kg/h IVI (max 80mg/kg/d). Whole-bowel irriga- tion to clear non-absorbed pills. Support circulation. Vitamin K for coagulopathy. Opiates Symptoms Itch, nausea, miosis, CNS and respiratory depression, apnoea. Treatment ABC. Naloxone, eg 400mcg IM/IV every 2min until RR (max 10mg). Short t½, so toxicity can recur. Consider IVI. 'Take home' naloxone to prevent death if risk. Phenothiazines Includes chlorpromazine, prochlorperazine, promethazine, thioridazine. 827 Symptoms Hyperthermia, HR, labile BP, dystonia, confusion, seizures. Treatment ABC. Circulatory support with IV fluids. Cool. Acute dystonia: pro- cyclidine 5–10mg IM/IV. Treat seizures (p810–11). Neuroleptic malignant syndrome: hyperthermia, rigidity, extrapyramidal signs, autonomic dysfunction (labile BP, HR, sweating, urinary incontinence), confusion, coma, WCC, CK. Treatment: cool, benzodiazepines can help fever and rigidity, eg lorazepam 1–2mg PO/IV every 4–6h. Also bromocriptine 2.5mg 2–3/d. 19 Emergencies Carbon tetrachloride Present in industrial solvents. Exposure via ingestion, trans- dermal, or inhalation. Symptoms Nausea, gastrointestinal irritation, headache, dizziness, dyspnoea, drowsiness, tachycardia, tachypnoea, liver and kidney toxicity. Treatment Remove clothing, irrigate eyes. Supportive. Case reports of treatment with antioxidants, eg methionine, acetylcysteine. Hyperbaric O2 if severe exposure (before liver dysfunction as oxidative processes may contribute to liver toxicity). Organophosphates Insecticides and chemical warfare. Rapidly absorbed via skin, mucous membranes, inhalation. Main concern is respiratory failure from excess secretions. Symptoms Inactivates acetylcholinesterase, leading to an increase in acetylcho- line and muscarinic SLUDGE effects: Salivation, Lacrimation, Urination, Diarrhoea, GI upset, Emesis. Also: diaphoresis, diarrhoea, miosis, bradycardia, bronchospasm, fasciculation, paralysis. Treatment PPE. Remove soiled clothes, wash skin. Atropine 1–2mg IV every 3–5min aiming for control of respiratory secretions and oxygenation. Pralidoxime (binds to organophosphate and reactivates acetylcholinesterase) may help paralysis (but not respiratory effects so give with atropine), eg 1–2g (20–40mg/kg) IV over 15–30min, repeat in 1h, then repeat every 3–8h depending on weakness. See also p830. Paraquat Found in weed-killers, contaminated cocaine. Diagnosis: blood/urine concentration. Symptoms D&V, painful oral ulcers, alveolitis, kidney/liver/heart failure, coma. Treatment Activated charcoal. Supportive. No antidote available. Excess oxygen may worsen lung toxicity. Ecstasy = 3,4-methylenedioxymethamphetamine (MDMA). Symptoms Nausea, muscle pain, blurred vision, amnesia, fever, confusion, ataxia, tachyarrhythmias, hyperthermia, hyper/hypotension, water intoxication, DIC, K+, AKI, hepatocellular and muscle necrosis, cardiovascular collapse, ARDS. Treatment No antidote available. Supportive: activated charcoal, cooling, IV fluid resuscitation. Benzodiazepine for agitation/seizures (pp810–11). Treat hypogly- caemia (p818), K+ (p297), narrow complex tachycardia (p790–1), hypertension (p778). Consider dantrolene for hyperthermia, eg 2–3mg/kg, then 1mg/kg repeated if necessary (max 10mg/kg). Snake bite (envenomation) Symptoms BP, swelling spreading proximally within 4h of bite, compartment syn- drome, bleeding gums or venepuncture sites, D&V, ptosis, trismus, rhabdomyolysis, kidney failure, pulmonary oedema, shock. 20-minute whole blood clotting test if limited access to laboratory facilities: collect 2–3mL of venous blood into a clean, dry test tube, leave for 20 minutes at room temperature. Unclotted blood or a friable clot that breaks down on tipping indi- cates a possible clotting disorder. Management ABC. Immobilize to reduce venom spread. Avoid tourniquet due to risk of local gangrene. Antivenom (if available) if shock, coagulopathy, neurotox- icity, AKI (black urine), rapidly progressive local swelling, bites known to cause local necrosis, or digital bites. Also tetanus toxoid (once coagulopathy corrected). Monitor for adverse reaction to antivenom (3–80% depending on dose/quality). Treat anaphylaxis (p776). 828 Burns Assessment Burn size is proportional to the inflammatory response (vasodilation, increased vascular permeability) and thus fluid shift from the intravascular volume. Calculate burn as % of total body surface area using a Lund and Browder chart (fig 19.30), or the ‘rule of nines’: Head and neck: 9%. Arm: 9%. Front of trunk: 2 ≈ 9% = 18%. Back of trunk 2 ≈ 9% = 18%. 19 Emergencies Each leg 2 ≈ 9% = 18%. Perineum 1%. Burn depth determines healing time/scarring. Assessment is hard, even with ex- perience. Burns can also evolve, particularly over the first 48h. Distinguish: Partial-thickness burns: painful, red, and blistered. Full-thickness burns: insensate/painless; grey-white. Management Resuscitate Airway: beware of upper airway compromise if hot gases inhaled. Suspect if his- tory of fire in enclosed space, soot in oral/nasal cavity, singed nasal hairs, or hoarse voice. Flexible laryngoscopy/bronchoscopy can be used to diagnose upper airway injury and inform intubation decision. Involve anaesthetists early. Monitor: ob- struction can develop in the first 24h. Breathing: exclude life-threatening chest injuries (eg tension pneumothorax) and constricting burns. Consider escharotomy if circumferential chest burns are impairing thorax excursion (OHCS p598). Suspect carbon monoxide poisoning from history, cherry-red skin. If COHb >10%, treat with 100% O2 (p826). Circulation: >15% partial-thickness burns require IV fluid resuscitation. Use 2 large-bore (14–16G) IV lines, through burned skin if needed, or intraosseous (see OHCS p182). Use a burns calculator or formula to determine amount of IV fluid needed, eg Parkland formula: 4 ≈ weight in kg ≈ % burn = mL of crystalloid needed in first 24h, half given within 8h. Replace fluid from the time of burn, not from the time admitted. Formulae are only guides: adjust IVI according to clinical response and urine output (aim ≥0.5mL/kg/h). Beware of over-resuscitation (‘fluid creep’) which can lead to complications, eg abdominal compartment syndrome. Disability: assess GCS. Consider carbon monoxide toxicity (p826), cyanide toxicity (p826), and trauma. Immediate burn management ‘Cool the burn, warm the patient.’ Remove burned/constricting/contaminated clothing unless molten/adherent. Cool the burn within 3h with cold water (not ice or iced water), or use a cooled, clean compress. Aim for 20 minutes of cooling. Cover non-burned areas, and keep these areas warm during cooling of burns. Cover burns with saline gauze. Specialist dressings may be available. Cling film can be a useful temporary measure and relieve pain. Do not burst blisters. Analgesia. Paracetamol, NSAIDS, codeine. If severe pain: Entonox®, titrate IV mor- phine until pain controlled. Surgical/plastics input. If circumferential burn of chest or limbs (above wrist/ ankle) refer for escharotomy/fasciotomy. Ensure tetanus immunity. Burns unit care Burns unit specialist advice ± transfer care if: Total body surface area burnt >10%, or full-thickness burn >5%. Airway compromise/inhalation injury. Circumferential burns to trunk or limbs requiring escharotomy. Chemical/high voltage electrical burn. Special area burns: hands, face, neck, feet, perineum/genitalia, joint affecting mobility.  A 829 A 1 1 2 2 2 2 13 13 1 1 19 Emergencies 1 1 1 1 1 2 2 1 B 1 B B B C C C C 1 1 1 1 Relative percentage of body surface area affected by growth Area Age 0 1 5 10 15 Adult A: half of head 9 8 6 5 4 3 B: half of thigh 2 3 4 4 4 4 C: half of leg 2 2 2 3 3 3 Fig 19.30 Lund and Browder chart for estimating the total body surface area affected by burns. 830 Hypothermia Have a high index of suspicion and a low-reading thermometer. Definition Core (rectal) temperature