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.
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An elderly female was admitted under the care of the orthopaedic team with a 2 week history of decreased mobility due to right knee pain. She had a past medical history of chronic atrial fibrillation, treated with amiodarone, and asthma which was well controlled on salbutamol inhalers. She was not on warfarin. Bony injury was ruled out clinically and radiologically and she was treated with simple analgesia. Whilst on the ward, she deteriorated acutely after complaining of shortness of breath. A cardiac arrest call was put out.
On arrival of the cardiac arrest team, she had a cardiac output. On examination, she was hypotensive (BP 70/50 mmHg) with a heart rate of 55 bpm. She was markedly cyanosed with a respiratory rate of 30 breaths per minute with oxygen saturation of 75% on high flow oxygen through a reservoir bag. Her Glasgow Coma Score was 7 (E1V2M4). There was no evidence of calf swelling or tenderness. Arterial blood gas analysis revealed marked type 1 respiratory failure – pH 7.2, pO2 5.4kPa, pCO2 7.8kPa, HCO3 19mmol/l and lactate 4mmol/l .
She was rapidly intubated, and resuscitated with a total of four litres of crystalloids and colloids. Invasive blood pressure monitoring was established. A clinical diagnosis of acute pulmonary embolus was made. She remained unstable despite resuscitation, requiring frequent boluses of vasopressors and adrenaline thus being too unstable to be transferred for a CT pulmonary angiogram. A bedside echocardiogram showed a markedly dilated right heart with elevated right heart pressures. There was paradoxical movement of the interventricular septum. Left ventricular function was also slightly impaired.
It was decided to thrombolyse the patient. As alteplase was being readied, the patient arrested. The initial rhythm was pulseless electrical activity with a rate of 40 beats per minute. She was resuscitated as per Advanced Life Support (ALS) guidelines and received adrenaline and atropine intravenously. After two cycles of cardio-pulmonary resuscitation (CPR) and the administration of thrombolysis, she regained cardiac output but remained hypotensive and hypoxic. An adrenaline infusion was commenced through a peripheral line. Despite this, she arrested six further times with increasing inotropic support requirement. After two hours from the initial cardiac arrest call, the decision was made to stop resuscitation.
Post-mortem results confirmed the presence of a large pulmonary embolus as well as bilateral deep venous thromboses (DVTs).
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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 63 yr old woman collapsed at home and was brought into ED with a GCS of 3/15. She was a known hypertensive and hypercholesterolaemic. CT scan revealed a Fisher grade 3 subarachnoid haemorrhage. A ruptured middle cerebral artery was secured 24 hours later. She extubated on day 3 with a GCS of 13, but dropped her GCS to 10 on day 5 and was treated for vasospasm, which included continuing the nimodipine and simvastatin from her admission.
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A 48 year old lady was admitted to critical care whilst suffering from sepsis secondary to severe cellulitis of her leg. She was obese with a BMI of 38 and was managed with insulin and oral anti-hyperglycaemics for type 2 diabetes mellitus. A doppler scan was unable to exclude a DVT. She had a further deterioration 30 hours later. Her sinus tachycardia accelerated to 130 bpm, along with a drop in blood pressure to 100/40. Arterial blood gas demonstrated an increasing A-a gradient as his FiO2 increased. Although such changes can occur in sepsis, the acute onset led to concerns regarding venous thromboembolism and pulmonary emboli.
What are the options for prevention of venous thromboembolism and pulmonary embolism?
A 34 year old IV drug abuser was admitted with respiratory failure, bilateral patchy changes on chest X-ray, raised inflammatory markers and septic shock. She was intubated and commenced on antibiotics and noradrenaline. An in-house Focussed Intensive Care Echo was performed to guide fluid resuscitation. This was suggestive of hypovolaemia, but a large mobile mass was also observed in the left ventricular chamber. A departmental echo the next day confirmed the presence of a large vegetation on the anterior mitral valve leaflet with severe mitral regurgitation. She underwent a further period of stabilisation and underwent a mitral valve replacement.
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An elderly man presented with an acute abdomen. At operation, he was found to have four-quadrant peritonitis due to a perforating sigmoid tumour. He underwent a hemicolectomy and had a defunctioning stoma formed. Postoperatively, he required 0.7mcg/kg/min noradrenaline to maintain a MAP 65mmHg. A vasopressin infusion was commenced and his noradrenaline requirements decreased. However, he developed acute kidney injury and subsequent multiorgan failure. Treatment was withdrawn around 48 hours post-operatively.
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A 65 year old chronic hypertensive man underwent a bone marrow transplant for acute myeloid leukaemia. He was subsequently treated for neutropaenic sepsis. He developed acute confusion and a subsequent drop in GCS requiring intubation. CT head and CSF investigation was normal. EEG was non-diagnostic. He was persistently hypertensive on the ICU. Review of notes showed that his anti-hypertensive medications had been omitted since admission, and that his ward blood pressures had been persistently elevated. Antihypertensives were established and the blood pressure improved. The neurological features improved with the blood pressure. A subsequent MRI confirmed the diagnosis.
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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?
A 40 year old woman presented with 4 days of abdominal pain, distended abdomen and faeculent vomiting. She was in septic shock on presentation and laparotomy revealed a sigmoid perforation with four quadrant peritonitis. Postoperatively she was extubated, but dependent on noradrenaline. Overnight, her vasopressor requirements escalated despite additional fluid resuscitation. Transthoracic echo suggesed hypovolaemia, and as she was hypoalbuminaemic she was given regular boluses of 20% albumin which resulted in transient improvments in blood pressure. Despite a return to theatre for further washout, she developed multiorgan failure and died.
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