A 40 year old woman was admitted to the emergency department (ED) after a syncopal episode. On admission she was in acute respiratory distress and described a two day history of sudden onset breathlessness. She had no previous medical history. Her only regular medication was the oral contraceptive pill. She had had a recent flu-like illness and been less active than usual. On arrival she had a respiratory rate of 30 breaths/minute with accessory muscle use. An ABG on 15L/min oxygen via non-rebreathe mask showed type I respiratory failure (PO2 8.4kPa). She was tachycardic (120bpm) and blood pressure was 98/50. Chest x-ray and bloods were unremarkable although her ECG revealed a sinus tachycardia with right axis deviation, Q waves and inverted T waves in lead III.
The patient had a bedside echocardiogram that revealed a severely dilated right ventricle with poor tricuspid annulus planar systolic excursion (TAPSE). A presumed diagnosis of a pulmonary embolism (PE) was made. Thrombolytic therapy was considered but rejected at this point, in view of the haemodynamic stability. The patient was commenced on enoxaparin at a dose of 1.5mg/kg.
CT pulmonary angiography confirmed the presence of bilateral pulmonary emboli. On return from CT the patient was sat up briefly at which time she became cyanotic and had a brief self-terminating seizure. During this time her blood pressure was not recordable, and significant hypotension secondary to obstructive shock was assumed to be the cause. At this point it was decided to proceed with thrombolysis. The patient was transferred to the Intensive Care Unit, made a rapid recovery without the need for vasopressors or intubation and ventilation, and was discharged from hospital a few days later.
What is the evidence for intravenous thrombolysis for intermediate-risk pulmonary embolism? Read More »
A 70 year old woman suffered an out of hospital cardiac arrest whilst playing golf. She received bystander cardiopulmonary resuscitation and two shocks from an automated external defibrillator which restored spontaneous circulation. She was intubated at the scene and arrived in the resuscitation department cardiovascularly stable, well oxygenated and unconscious in the context of propofol sedation.
There was no prodrome suggestive of a specific aetiology for the cardiac arrest but information from relatives described an ex-smoker with hypercholesterolaemia and diet controlled diabetes mellitus who had previously undergone percutaneous coronary intervention (PCI) for ischemic heart disease. She took regular aspirin, statin and beta-blocker. A post resuscitation 12 lead ECG showed sinus rhythm, left axis deviation and non-specific lateral ischaemia. Troponin was elevated above 200 ng/L.
In view of this she was loaded with dual antiplatelet therapy and underwent emergency coronary angiography which demonstrated occlusion of two small branches (OM1 and PLV) but no large vessel coronary artery occlusion to explain the cardiac arrest. The occluded vessels were not stented. Subsequent echocardiogram and cardiac MRI demonstrated old circumflex territory scar but an otherwise normal heart and ultimately it was agreed that the cause of cardiac arrest was probably ventricular arrhythmia secondary to scar.
She was ventilated for 24 hours with targeted temperature management before being woken and extubated. Although she was initially confused, her neurology improved over approximately 48 hours such that she was discharged with no apparent neurological injury. An implantable cardiac defibrillator was placed prior to discharge to prevent sudden cardiac death from any future arrhythmia.
In survivors of out of hospital cardiac arrest should we proceed to early coronary angiography with a view to PCI?
If so, should we apply this approach to all such patients or only a subset?
If we do proceed to early coronary angiography, should this occur before or after other investigations, specifically computed tomography (CT) of the head and chest to look for intracerebral bleed and pulmonary embolism?
A 35 year old male presented with massive (over 1500mg) propranolol overdose on a background of depression and anxiety. He called for help and was found alert and cardiovascularly stable by paramedics at 50 minutes post ingestion. By 80 minutes his conscious level had fallen to a Glasgow Coma Score of 11 and he had become hypotensive. He started fitting en route to hospital and lost cardiac output as he arrived at hospital. The initial cardiac arrest rhythm was broad complex slow pulseless electrical activity. After a prolonged resuscitation attempt he regained spontaneous cardiac output but never achieved cardiovascular stability and sadly died later that evening.
He was resuscitated according to standard resuscitation algorithms. In addition, several specific therapies were given in line with Toxbase recommendations1: Glucagon was administered as a 10mg slow bolus followed by a 100-150 mcg/kg/hr infusion. Insulin (actrapid) was given as a 60 unit bolus followed by a 1-2 unit/kg/hr infusion along with a glucose bolus of 0.5 g/kg followed by an infusion of 0.5 g/kg/hr. Intralipid was delivered as a bolus (100 ml 20%) followed by an infusion. Atropine 3mg was given and the adrenaline boluses were changed to an infusion at 10 mg/hr.
Cardiac arrest remained refractory until a 100 ml bolus of 8.4% Sodium Bicarbonate was administered prompting almost instantaneous restoration of circulation.
The circulation remained unstable with a broad complex bradycardia resistant to transcutaneous pacing. High dose adrenaline infusion, high dose euglycaemic insulin therapy and glucagon infusion were continued. Transvenous pacing was also ineffective and the patient sadly deteriorated into a refractory cardiac arrest from which he did not recover.
The patient regained his cardiac output when the sodium bicarbonate bolus was given. The temporal association between these two events was profound and led me to question why this therapy sits so far down the toxbase treatment algorithm.1
A previously healthy 58-year-old male was admitted to hospital following an OOH cardiac arrest. The initial cardiac rhythm was VF. He remained on the ‘shockable’ side of the ALS algorithm and was managed accordingly with defibrillation and intravenous adrenaline. ROSC occurred after 28 minutes. A 12-lead ECG showed a STEMI in the antero-septal territories.
Coronary angiography showed a proximal occlusion of the left anterior descending artery through which a drug eluting stent was inserted. Despite this and adrenaline (10-20mcg) boluses, the patient remained persistently acidotic and hypotensive. A diagnosis of cardiogenic shock was made and an intra-aortic balloon pump (IABP) was inserted via the left common femoral artery with subsequent improvement in haemodynamic parameters. The patient was transferred to a cardiothoracic critical care.
Transthoracic echocardiography showed a globally hypokinetic left ventricle (LV) with an ejection fraction (EF) of approximately 20%. Within the first 6 hours, he developed runs of non-sustained VT and frequent ventricular ectopics, which interfered with IABP triggering causing worsening haemodynamic instability. Triggering was switched from ECG to arterial pressure. Electrolytes were supplemented and intravenous amiodarone was commenced to manage the dysrhythmias. Targeted temperature management to 36 degrees Celsius for 24 hours was initiated. Anticoagulation for IABP was commenced and peripheral pulses were regularly monitored.
His dysrhythmias resolved with subsequent improvement of IABP performance. On day 3, the IABP was weaned to 1:2 ratio for approximately 6 hours and removed. A tracheostomy was inserted on day 7 and the patient underwent long term respiratory wean and neurological rehabilitation.
Describe the indications, contraindications, complications and basic principles of intra-aortic balloon counterpulsation balloon pump.Read More »
A 50 year old man was found by the roadside by paramedics with a GCS of 13. On arrival he had a patent airway, but a GCS of 5 (E1 M3 V1). He had an elevated respiratory rate (30/min) and a profound metabolic acidosis (pH 6.97 pO2 16.8 pCO2 1.68 HCO3 2.8 BXS -30.8 COHb 0). The lactate was too high to be measured by the blood gas analyser and there was an elevated anion gap [(147+5.5) – (2.8+ 109) = 40.7] He was cardiovascularly stable with warm peripheries. His ECG revealed a prolonged QTc. He was intubated and 8.4% sodium bicarbonate was administered. His initial laboratory bloods showed CRP 11, white cell count 29.5 CK 2539 creatinine 213. Ethanol levels were <10 and Paracetamol and salicylate levels were within normal limits. He was given a dose of intravenous cefotaxime and his urine was sent for organic acids screening which revealed an enormous peak of glycolic acid and small increase in oxalic acid, consistent with an overdose of ethylene glycol.
After arrival in intensive care, the sodium bicarbonate had improved the pH to 7.2, with a residual lactaemia (15 as measured in the laboratory, without any interference from glycolic acid). CVVHDF was commenced. In order to inhibit futher metabolism of the ethylene glycol, 10% ethanol was commenced until fomepizole was available (an initial bolus of 800ml, followed by an infusion at 180ml/hr). Ethanol levels were monitored. Fomepizole was administered later that day abd the ethanol stopped (15mg/kg loading and 1mg/kg/hr). The renal function deteriorated despite CVVHDF (peaked at urea 28, creatinine 724 on day 4), which was continued for 5 days. Treatment for aspiration pneumonia was started in day 1 and cardiovascular support was continued (noradrenaline). Intermittent boluses of glycopyrolate were required to treat the bradycardia associated with fomepizole. A gradual improvement occurred and he had made a full neurological recovery within 2 weeks, with much improved renal function. He later admitted to drinking 250ml of antifreeze.
What are the clinical features and management of ethylene glycol poisoning?Read More »
A 44-year-old lady was brought to ED by ambulance after her partner found her drowsy in her bedroom with multiple empty packets of Amitriptyline scattered around the bed. The ambulance crew found no other medications in the immediate vicinity. Her partner had last seen her two hours previously that evening and described a history of depression, previous overdoses and chronic alcohol excess. On arrival in ED, her airway was self-maintained but she had signs of vomitus around her mouth and smelled strongly of alcohol. Heart rate was 125, NIBP 92/38 and ECG showed sinus rhythm with prolonged PR and QRS intervals (240ms and 200ms, respectively). ABG showed a metabolic acidosis with lack of respiratory compensation, with hyperlactataemia (4.1). GCS was 9 (E2M5V2) although she appeared agitated with bilaterally dilated pupils. There was no external evidence of injury. The impression was of life-threatening Tricyclic Antidepressant (TCA) overdose within the last 2 hours along with alcohol ingestion.
What are the main features of a Tricyclic Antidepressant overdose? What treatment options are available?
A 40 year old man with pre-existing mental health problems presented after an overdose of 6g of amitriptyline. He was deeply unconscious and required invasive ventilation. He was commenced on bicarbonate therapy and hyperventilated to pH 7.5. Around 12 hours after admission he developed tonic-clonic seizures, a broad complex tachycardia and subsequently suffered a cardiac arrest that was refractory to defibrillation, adrenaline and amiodarone. He was given additional 8.4% bicarbonate and further defibrillation attempts and was successfully resuscitated after 90 minutes.
What is the rationale for the use of sodium bicarbonate in the management of amitriptyline overdose?Read More »