Massive Propranolol Overdose

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

This case summary aims to answer: 

  1. What works in Propranolol overdose? 
  2. What doesn’t really work? 
  3. Which order should I give things?

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Management of Inhalational Injury

A 30-year-old man with no significant past medical history was admitted to ED from a house fire started by a piece of faulty electrical equipment. There were superficial skin burns only but some evidence of a possible inhalation injury with singed nasal hairs and a hoarse voice. Coughing resulted in expectoration of carbonaceous sputum with some haemoptysis. Arterial blood gas analysis revealed a PaO2 of 10.4 kPa on 40% oxygen a carboxyhaemoglobin level of 18%.

Semi-elective endotracheal intubation was performed using an uncut orotracheal tube. Ventilatory parameters were adjusted to give a tidal volume of 6-8 ml/kg and plateau pressure of less than 30 cmH20. Recruitment manouveres were performed to give an optimum compliance in the region of 40-50 ml/cmH20 with a positive end-expiratory pressure of 8 H20. The inspired fraction of oxygen was kept high (i.e. greater than 60%) until there was a fall of the carboxyhaemoglobin level to less than 5% at which point downwards titration was performed as guided by a target SpO2 of 94%.

Fibreoptic bronchoscopy was performed approximately six hours after admission to intensive care which demonstrated carbonaceous colonisation of the lower respiratory tract and areas of erythematous and denuded epithelium. Within 12 hours of intubation significant oedema of the face and upper airway had developed. A restrictive fluid regimen was instituted and there was gradual resolution of this swelling over the next 3 days. At this time, gas exchange was satisfactory and the patient was successfully extubated before being discharged to the high-dependency unit.

How is inhalational injury managed on the ICU?Read More »

High Dose Insulin Infusion for Calcium Channel Blocker Overdose

A 24-year-old was admitted following an intentional overdose of 10mg amlodipine tablets following an argument with his family. Approximately 10 tablets were ingested. On self-presentation two hours after the event, he was clinically stable with no haemodynamic compromise. There was no airway or respiratory compromise and a 12 lead electrocardiogram demonstrated sinus rhythm at 98 beats per minute. Both an arterial blood gas and electrolyte analysis were normal. Ionised calcium was 1.14 mol/L.

Over the following two hours he developed hypotension down to a nadir of 58/32 mmHg without change in heart rate or rhythm or the development of metabolic abnormalities. This was initially treated with intravenous fluids without significant response. A bolus of calcium chloride was administered without success; at this time he was referred to the intensive care team for assessment. Careful clinical examination revealed no other abnormality except hypotension. Neurological function remained intact and there appeared to be a vasodilated state with warm peripheries and relative tachycardia at 110 beats per minute in sinus rhythm.

The patient was transferred to the intensive care unit where an infusion of noradrenaline was commenced, rapidly escalating to a rate of 0.92 mcg/kg/min with little improvement in mean arterial pressure beyond 30-40 mmHg and relative oliguria. After consultation with the National Poisons Service, a high dose infusion of actrapid was commenced at rate of 0.5 units/kg/hour, with subsequent improvement of his haemodynamic parameters and a reduction in his noradrenaline requirement. Over the following 4 hours, both this infusion and the noradrenaline infusion were subsequently weaned off. The patient was discharged to the ward after eight hours and after assessment by the psychiatric team, from hospital the following day.

What are the clinical features of calcium channel blocker overdose and what is the role of high dose insulin infusion?Read More »

Attempted Suicide and Treatment Withdrawal

A elderly man  was found unconscious at home having taken an overdose of prescription medication. This event may have been precipitated by a recent bereavement and worsening of his preexisting depression for which he had recently been reviewed by psychiatric services and commenced on an SNRI. He left a note at the scene of the suicide attempt, clearly stating that he intended to take his own life and did not wish to be resuscitated in the event of being found alive. He was discovered in his home by a relative who had been growing increasingly concerned as to his welfare, having not spoken to him for several days. On arrival in ED his Glasgow coma score (GCS) was 3/15. He was known to be taking venlafaxine for depression and amitriptyline for chronic back pain, and empty packets of each drug were found at his home.

He was intubated and transferred to the intensive care unit. Supportive care was provided including vasopressors (noradrenaline) for hypotension, electrolyte correction and ventilatory support. Plain chest radiograph showed a probable aspiration pneumonitis affecting the right upper and middle lobe. He was hypoxic with a high Fi 02 requirement and needed high levels of PEEP to maintain adequate oxygenation. His conscious level fluctuated over several days and he became increasingly agitated and exhibited signs of distress. At this stage it was not clear if he was orientated in time, place or person. He underwent percutaneous tracheostomy to facilitate weaning and reduce sedation requirements.

We were then able to wean him from sedation by day 11 of his admission. The patient’s ventilatory requirements were still high requiring mean airway pressures of 30 cmH2O, PEEP of 10 cmH2O, and an inspired oxygen concentration of 60%. At this stage he indicated to the ITU team that he did not wish treatment to be continued. We found him to be fully orientated in terms of time and place and he was aware of the preceding events and his intentional overdose. It was clearly explained to him that if treatment were discontinued he would die. He indicated to us that he had no intention of changing his mind.

We referred him to the liaison psychiatrist for the hospital who independently assessed and found him to be competent and able to fully understand the implications of such a decision, i.e. his likely death from respiratory failure. The psychiatrist also found him to be depressed but noted that this did not interfere with his competence and ability to give or withhold his consent. With his consent, his family were informed of this development. They had been agonizing for some time over whether they had made the right decision to call emergency services when they first found him. They attempted to dissuade him but his resolve was unshakeable. Invasive ventilation was withdrawn on the morning of his 15th day of ITU as per his wishes. Diamorphine was administered to reduce symptoms of respiratory distress. He died of hypoxia later that day. Cause of death was recorded as aspiration pneumonia.

Describe the ethical and legal framework utilised in the management of this patient.Read More »

Ethylene Glycol Poisoning

Ethylene Glycol Poisoning

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 »

Management of Life-Threatening Tricyclic Antidepressant Overdose

Management of Life-Threatening Tricyclic Antidepressant Overdose

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?

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Sodium Bicarbonate in Amitriptyline Overdose

Sodium Bicarbonate in Amitriptyline Overdose

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 »



A young female IV drug abuser presented with dysarthria, diplopia and weakness with loss of her gag reflex. She had recently had an abscess wound on her arm debrided. She was intubated for airway protection, and underwent early tracheostomy. She was treated with intravenous antibiotics and botulism antitoxin after electromyography and nerve conduction studies were consistent with a diagnosis of botulism. She was weaned from the ventilator within 2 weeks and the Health Protection Agency later confirmed the presence of botulism neurotoxin A from wound swabs.

What are the clinical features of Botulism and how is it managed?Read More »

Intralipid in Antihypertensive Overdose

Intralipid in Antihypertensive Overdose

A middle aged man presented after having taken a mixed antihypertensive overdose of ramipril, amlodipine and bendroflumethiazide. He had refractory hypotension despite fluids, noradrenaline, adrenaline vasopressin and calcium infusions.  After discussion with toxicologists he was given 20% intralipid as per the AAGBI guidelines for LA toxicity. There was an immediate but transient improvement in his BP with two bolus doses of intralipid. Over the subwequent hours and days, he stabilised and weaned off his vasopressor support. There was no long-lasting organ dysfunction.

What is the evidence for the use of intralipid in the management for antihypertensive overdose?

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