Category: 4.1

Prescribes drugs and therapies safely

Heparin Induced Thrombocytopaenia

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A 75 year old was admitted to the Cardiac Intensive Care Unit following aortic valve replacement for severe aortic stenosis. He had no other significant past medical history. He remained intubated and ventilated overnight until cardiovascularly stable, and was extubated the following morning. He suffered bleeding into the pericardial drains, and went back to theatre on day 3. He remained intubated on his return from theatre. On day 7 it was noticed that he had developed thrombocytopenia, with a platelet count of 34, reducing from 103 the previous day. A heparin induced thrombocytopenia (HIT) screen was sent, and he was changed to alternative anticoagulation.

The HIT screen was positive. His platelet count fell further and he continued to bleed slowly from any puncture sites and from around his mouth and gums. He remained intubated and ventilated and developed a requirement for inotropic support. Transfusions of platelets were required for any intervention. He was anticoagulated with lepirudin to prevent thrombosis. His platelet count continued to remain in single figures over the next 10 days despite treatment with steroids. Unfortunately he deteriorated, suffering an arterial thrombosis in his arm, renal failure and developed a necrotic skin rash all over his body, likely to be related to the HIT. Following discussions with his family, who felt he was suffering and would not want a poor quality of life, treatment was withdrawn on day 26 of his intensive care stay and she died.

What are the clinical implications of heparin-induced thrombocytopaenia?Read More »

Transplantation After Brainstem Death

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A 38-year-old previously fit man suffered a grade five subarachnoid haemorrhage. Attempts at coiling failed and he suffered a catastrophic rebleed on-table whereupon his pupils became fixed and dilated. After a suitable sedation washout period he underwent testing which confirmed brainstem death at which point he was referred to the specialist nurse for organ donation. Following counselling of the family and appropriate assessment, donation of his kidneys, liver and heart was agreed.

Upon confirmation of brainstem death, mechanical ventilation was continued to ensure PaO2 greater than 10 kPa and limit peak inflation pressure to less than 30 cmH20. Vasoactive support was switched from noradrenaline to vasopressin 0.02 iu/kg/min. Methylprednisolone and intravenous triiodothyronine were administered whilst awaiting harvest. Blood antibody testing for HIV1+2, Hepatitis B and C, HTLV-1 and CMV IgG were all negative. A transthoracic echocardiogram confirmed good biventricular function; following discussion with the transplant retrieval team a pulmonary artery catheter was floated. Clinical measurements of cardiac output and mixed venous oxygen saturation were satisfactory. Adequate hydration was maintained with crystalloid by infusion and glucose control optimised in the range 8-10 mmol/L with insulin. The dedicated retrieval team performed the organ retrieval eighteen hours after confirmation of brainstem death.

How can we optimise organ function for organ donation?Read More »

Use of Bicarbonate in Lactic Acidosis

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Five days post emergency colorectal surgery, an elderly woman, following a brief period of chest pain a few hours earlier, developed progressive hypotension and tachycardia on the ward. She had a background of hypertension, type 2 diabetes and a chronic left foot ulcer. On examination she was found to be clammy, mottled and peripherally vasoconstricted with a GCS of 15/15. Her abdomen was soft and non-tender. Her initial ECG had showed no ischaemic changes and subsequent ECGs showed only a sinus tachycardia.

Initial blood gas analysis showed a metabolic acidosis (pH 7.21 Lactate 2.8mmol/l, HCO3 11.1mmol/l with a pCO2 of 2.7kPa).  A starting differential diagnosis of a cardiac event, a pulmonary embolism, critical ischaemia or sepsis related to a hip or foot ulcer were made. Urgent orthopaedic and vascular review were obtained, and it was deemed that neither the hip, ulcer or vascular insufficiency were a likely source for the deterioration. Initially it was planned to transfer her for a CTPA, however she became progressively unstable, was no longer fluid responsive, and was intubated on the ward and transferred to the intensive care unit (ICU) for stabilisation.

On arrival on ICU she continued to deteriorate, and in addition to fluid resuscitation required a high dose noradrenaline infusion to maintain her blood pressure. Broad spectrum antibiotics were started, a bedside echocardiogram and blood tests performed and hydrocortisone started. Her metabolic acidosis continued to deteriorate, subsequent arterial blood gas showed a pH 6.91, Lactate of 13.7mmol/l, HCO3 7.7mmol/l, base excess -25mmol/l with a pCO2 of 5.4kPa. It was decided to correct this acidosis with a bicarbonate infusion and initially 200ml of 8.4% was given over an hour, based on correcting half the calculated bicarbonate deficit (bicarbonate deficit (mmol) = base deficit 0.3xbodyweight(kg)1).  The blood gas following this infusion showed improvement in the metabolic acidosis despite the increasing Lactate (pH 7.07, Lac 14.0mmol/l, HCO3 10mmol/l, BE -18.6mmol/l with a pCO2 of 4.85kPa). She continued to deteriorate and the results from her blood tests, troponin and bedside echo suggested a primary myocardial infarction to cause this decline. She was too unstable for primary coronary intervention and her condition continued to deteriorate. She died 6 hours post admission.

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High Dose Insulin Infusion for Calcium Channel Blocker Overdose

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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 »

Thrombolysis in Pulmonary Embolism

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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).

What is the evidence for the use of thrombolysis in pulmonary embolism?Read More »

Management of Variceal Haemorrhage

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A 60-year-old alcoholic was admitted with large-volume, frank haematemesis. On presentation he was hypotensive, tachycardic and obtunded with multiple stigmata of chronic liver disease including a moderate volume of ascites and palpable splenomegaly. Initial phlebotomy revealed a haemoglobin of 6.4 g/dL, INR of 4.5 and bilirubin of 54 μmol/L. Arterial blood gas analysis demonstrated a significant metabolic acidosis and lactate of 11 mmol/L. Large bore intravenous access was established and administration of crystalloid initiated, targeting a systolic blood pressure of 90 mmHg. Urgent cross-match of 10 units of packed red blood cells, clotting products and platelets was requested and the patient was transferred to theatre where upper gastrointestinal tract endoscopy was performed under general anaesthesia. This demonstrated three columns of varices involving the gastro-oesophageal junction. Attempts at banding and injection of sclerosant met with variable success. A Senstaken-Blakemore tube was inserted due to incomplete haemostasis and further attempts at endoscopic therapy abandoned.

The patient was transferred to intensive care. Intravenous cefotaxime and terlipressin were commenced. Further transfusion of clotting products continued as guided by thromboelastography with some slowing of transfusion but red cell requirements persisted at a rate of 1-2 units of blood per hour. At 12 hours, repeat endoscopy was performed – further attempts at sclerotherapy were unsuccessful and transjugular intrahepatic porto-systemic shunting was performed by the interventional radiology team. Upon return to intensive care, a significant reduction in bleeding was noted and both haemodynamic indices and coagulopathy improved over the following 12 hours. A repeat endoscopy demonstrated no evidence of active ongoing bleeding. At this point sedation was stopped; some encephalopathy was evident although this improved in the following 24 hours. Extubation occurred on day 3 after admission and he was discharged to the high-dependency unit at day 5 without significant ongoing acute issues.

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Secondary Complications of Subarachnoid Haemorrhage

Secondary Complications of Subarachnoid Haemorrhage

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A thirty eight year old female smoker was admitted via A+E following sudden onset occipital headache with visual disturbance and collapse with loss of consciousness lasting approximately five minutes. She had complained of unusual headaches a week prior to this event, but these were short lived and not associated with any neurology. On arrival in resus she had recovered to a Glasgow coma score (GCS) of 14/15. She demonstrated neck stiffness and photophobia, as well as general irritability. Plain computerised tomography
scan (CT) performed showed a subarachnoid haemorrage in the region of the middle cerebral artery, with the presence of blood in the sylvian fissure.

She was transferred to the ITU for monitoring and blood pressure control with invasive arterial and central venous pressure monitoring. She was treated with nimodipine to prevent vasospasm. Contrast CT performed showed an aneurysm at the bifurcation of the middle cerebral artery, and this was felt to be the origin of the bleed. She underwent uneventful endovascular coiling of this aneurysm the following day under general anesthesia, and was discharged to the neurosurgical team for ongoing care afterwards.

What are the secondary complications of subarachnoid haemorrhage and how are they managed?

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Invasive Streptococcal A Infections and Intravenous Immunoglobulin

Invasive Streptococcal A Infections and Intravenous Immunoglobulin

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A middle aged woman presented with a one day history of swollen, painful red thigh after a prodromal sore throat. She had a exquisitely tender left thigh and knee with cellulitis. She was apyrexial, with normal heart rate and blood pressure, but had a respiratory rate of 24. She had a neutrophilia (28), elevated CRP, hyperlactataemia (4.1) an acute kidney injury (creat 170) and a mild coagulopathy. She was given analgesia, broad spectrum antibiotics (including clindamycin) and underwent a CT thigh which showed muscle swelling in the anterior compartment with fluid tracking up to the hip. Knee aspirate showed large number of gram positive cocci, later confirmed as Streptococcus A. Two hours into her admission the inflammation was involving the groin. She underwent exploration and debridement in theatre, and was noradrenaline dependent postoperatively. She was commenced on intravenous immunoglobulin on the same day. She required further debridement of the leg and lower abdomen on day 3. She gradually weaned off support, and underwent several more operations for closure of wounds and reconstructive surgery.

What is the role of IVIG in Invasive Streptococcal Infections

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Hypertonic Saline for Raised Intracranial Pressure

Hypertonic Saline for Raised Intracranial Pressure

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A 40 year old male was brought into ED following a high speed road traffic accident. The patient was ejected from the vehicle. The patient was managed according to ATLS guidelines. He suffered extensive injuries including facial fractures, traumatic subarachnoid haemorrhage and multiple intra-cerebral haemorrhages, a flail chest and thoracic and cervical spine injuries. Once stabilised, the patient was transferred to the neurosurgical intensive care unit where an intra-cranial pressure (ICP) monitor was inserted to measure intracranial pressures. His ICP was persistently raised despite optimising respiratory parameters, deep sedation, muscle relaxation and then mannitol. A decision was made to commence an infusion of hypertonic saline 2.7% according to the local protocol. The ICP improved rapidly and stabilised and removed the need to proceed with surgical decompressive craniotomy.

What is the evidence for the use of hypertonic saline in the treatment of acutely raised intracranial pressure?Read More »

Dexamethasone in Bacterial Meningitis

Dexamethasone in Bacterial Meningitis

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A previously healthy 25 year old female was admitted with low GCS and a fever. She had a 24 history of viral symptoms including sore throat and a headache. On admission she had a GCS of 3, temperature of 38.9°C and raised inflammatory markers. She was intubated but did not require vasopressor support. A CT brain showed diffuse cerebral swelling, effacement of the sulci, sylvian fissures, basal cisterns and 3rd/4th ventricles, and early cerebellar tonsillar herniation. Lumbar puncture was not performed due to CT appearances. She was commenced on intravenous (IV) ceftriaxone 2g twice daily, IV acyclovir 800mg three times daily, and IV dexamethasone 10mg four times daily. Unfortunately, her pupils remained fixed and dilated on sedation hold 36 hours later, and she was making no respiratory efforts. She subsequently became a DBD organ donor.

What is the evidence for dexamethasone in bacterial meningitis?

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