A 55 year old male presented with acute upper abdominal pain and haematemesis. He had admitted drinking alcohol to excess. Following admission, he had a further significant episode of haematemesis associated with haemorrhagic shock. An emergency oesophagogastrectomy (OGD) was arranged in theatre. His pre-procedure haemoglobin was 60g/L. OGD revealed large amounts of fresh blood in the stomach, which prevented identification of the bleeding point. The patient had a number of oesophageal varices, attempts were made to band these but this did not stop the bleeding. A partial gastrectomy was undertaken. The patient received a total of 18 units of red blood cells, 14 units of flesh frozen plasma and 2 units of platelets and cryoprecipitate before being taken to Intensive Care intubated and ventilated.
On the Intensive Care Unit he was warmed and repeat blood tests were sent to ensure correction of his coagulopathy. Haemoglobin was recorded as 9.4g/dL and the APTTr was normal. The following day when he was normothermic and cardiovascularly stable he was woken and extubated. He was discharged to the ward the following day.
When should we transfuse in upper gastro-intestinal haemorrhage? Are there any adjunctive therapies that can help?Read More »
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 »
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.
An 18-year-old known asthmatic presented with a two-day history of increasing shortness of breath on a background of a recent coryzal illness. She had a background of reasonably poor control and had been admitted to the intensive care unit for mechanical ventilation twice as a child. Her current medication included regular inhaled serotide 250, montelukast 10mg and theophylline MR 450mg BD. At presentation she was in extremis; pulse rate was 65 per minute, blood pressure 75/54 mmHg and respiratory rate 14 per minute. Arterial blood gas analysis demonstrated a PaCO2 of 11 kPa and PaO2 of 7.6 kPa with associated respiratory acidosis. Nebulised salbutamol and intravenous magnesium sulphate therapy was administered. along with 200mg of intravenous hydrocortisone. On arrival of the intensive care team, the patient’s respiratory rate deteriorated to a rate of 4 per minute. Assisted ventilation with a self-inflating bag and 100% oxygen was performed; rapid-sequence intubation was performed using ketamine and rocuronium.
Following intubation, immediate difficulties were experienced with mechanical ventilation. High airway pressures in excess of 40 cmH2O with tidal volumes of less than 200 ml were observed. Immediate chest radiography confirmed correct positioning of the endotracheal tube and excluded a pneumothorax. Adequate sedation and neuromuscular blockade were confirmed. Auscultation confirmed severe, widespread wheeze with limited air entry. Further nebulised salbutamol was administered and an aminophylline infusion initiated. The patient was transferred to the intensive care unit where magnesium, ketamine and vecuronium by infusion were added. Various modes of mechanical ventilation were tried including volume and pressure triggered with varying success; this included lengthening the I:E ratio, frequent disconnections to allow deflation and adjustment of PEEP to maximum compliance. Continuous salbutamol was administered via an ultrasonic nebuliser. Airway pressures remained high and there was little improvement in her acidosis. 2 hours after admission the patient suffered a PEA cardiac arrest from which she could not be resuscitated.
What are the difficulties in ventilating severe asthmatics, and what strategies can we use to overcome them?
A 40-year-old female intravenous drug user presented with a diffusely swollen right lower leg. She had injected heroin into her right thigh one week previously. The swelling started 3 days later. Initial observations revealed T 39.6, HR 135, NIBP 100/87, RR 32, Sats 96% on air. On examination, she was pale and sweaty. She had a swollen right lower leg with mottling of her foot and poor pedal pulses. Following initial fluid resuscitation, chest X-ray, cultures and broad-spectrum antibiotics (Flucloxacillin, Metronidazole and Gentamicin), she underwent CT angiogram of her lower limbs which showed oedematous and expanded muscle compartments of the thigh and calf but patent arterial flow to the feet. There was also right common femoral vein thrombosis with some vessel patency. Initial labs revealed neutrophilia (9.2), thrombocytopaenia (16) and deranged coagulation (PT 16, APPT 33, Fib 2.6). CK was 57000. She underwent right leg fasciotomies and was brought to ICU ventilated and on Noradrenaline to maintain MAP >65. She commenced Immunoglobulin IV 1gram/kg per day for 2 days for suspected Streptococcus Group A sepsis. That night she had massive transfusion requirements due to ongoing haemoserous ooze from her fasciotomy sites, losing up to 1 litre of haemoserous fluid per hour. Overnight she received 10 units RCC, 8 x FFP, 6 x Platelets and 2 x Cryoprecipitate, as well as Vitamin K (guided by Hb on ABG, formal lab results and thromboelastography). She was discussed with the Haematology Consultant and it was decided that, if rapid blood loss continued despite full correction of her clotting factors, fibrinogen and platelets then Factor VII could be given. However, over the next 2 hours, losses were much reduced following product replacement, and since she already had clot in her femoral vein, Factor VII Concentrate was not given.
What is the role of Recombinant Factor VIIa in major haemorrhage?
A 45 year old female presented to A&E with a 5 day history of worsening SOB, cough productive of green sputum, lethargy, anorexia, fever and rigors. She had no co- morbidities and was active and independent with a good exercise tolerance. On examination she looked unwell, clammy and drowsy. Her respiratory rate was 35 breaths per minute and SpO2 of 84% on 15 Litres of oxygen via a non-rebreathing mask. Her blood pressure was 88/40 mmHg with a heart rate of 140 per minute despite having received 3 litres of fluid. Arterial blood gas showed PaO2 6.0kPa, pH 7.28, PaCO2 7.1 kPa, Bicarbonate 14 mmol/l, BE -11 and Lactate 8.6 mmol/l. Chest radiograph demonstrated significant bilateral consolidation with infiltrates consistent with ARDS. PaO2:FiO2 was calculated as 15 indicating severe ARDS presumed secondary to CAP.
She was managed as per sepsis guidelines. Oxygen therapy was continued and CPAP was initiated due to the hypoxia whilst an ICU bed was being prepared for admission. Noradrenaline was commenced at 0.2mcg/kg/min which continued to increase. Repeat arterial blood gases confirmed worsening type 2 respiratory failure and the patient was clinically exhausted. A modified rapid sequence induction was performed and IPPV commenced. Her oxygenation remained a problem and despite a FiO2 of 1.0 and PEEP of 20 his SpO2 remained 85% and PaO2 6kPa. The patients’ sedation was deepened and muscle relaxant administered. Lung protective ventilation was continued however arterial blood gases continued to worsen. The decision was made to convert the patient from conventional ventilation (CV) to High-Frequency Oscillator Ventilation (HFOV). The initial ABGs after an hour of HFOV showed an improvement as did subsequent numbers. This mode of ventilation was continued for a further 48 hours and then converted to CV. Gas exchange continued to improve. Over the course of the following 4 weeks the patient had a tracheostomy performed to aid weaning. She subsequently developed a Ventilator Associated Pneumonia and worsening ARDS required a further period of HFOV. Improvement continued and the patient was successfully decannulated and discharged from ICU.
What is the evidence base for high frequency oscillatory ventilation in ARDS?
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?
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 forty-year-old motorcyclist was admitted to the ITU following a road traffic accident involving a stationary vehicle. She sustained a fractured right distal radius and multiple left sided rib fractures, involving ribs 2 to 9, with a free floating flail segment. She developed respiratory distress due to underlying lung contusions and a haemopneumothorax and was treated with two left sided intercostal drains, endotracheal intubation and invasive ventilation. She developed ARDS with bilateral infiltrates and PF ratio of <200mmHg, with normal cardiac function on transthoracic echocardiography. She was tracheostomised on day 12, and had a protracted ventilatory wean further complicated by a ventilator associated pneumonia. She was enterally fed during this period but began to develop an ileus and gut dysmotility, resistant to prokinetic treatment, leading to large volume gastric aspirates. She became visibly malnourished and was commenced temporarily on parenteral nutrition and IV glutamine. The ileus resolved over the following week and weaning recommenced, having ceased due to diaphragmatic splinting. She eventually weaned from the ventilator and was discharged from the ITU on day 40. She was profoundly weak due to a critical illness acquired weakness.
What is the role of glutamine supplementation in critical illness?Read More »
A 66 year old man was brought by ambulance to ED after becoming acutely dyspnoeic at home, and his wife had struggled to wake him after an afternoon sleep. He had a moderate smoking history of 20 pack years and quit 20 years ago, and drank approximately 20 units of alcohol as beer per week. There were no preceding prodromal respiratory or infective symptoms reported. On examination, he was obese with a weight of 120 kg. He was snoring, which eased with a chin-lift or jaw thrust, but he would not tolerate an airway adjunct. His respiratory rate was 8 and shallow, producing SpO2 84% on high flow oxygen. He was flushed and veno-dilated peripherally, with a tachycardia of 110 bpm sinus rhythm. Most notably, he was difficult to rouse, with a GCS of 9 (E2 M5 V2). Arterial blood sampling revealed a profound hypercapnoeic respiratory acidosis with no degree of compensation. Chest X-ray showed poorly expanded lungs with bilateral basal atelectasis and prominent pulmonary vasculature. Empiric naloxone was ineffective and he was commenced on non-invasive ventilation (NIV). The working diagnosis was an acute non-infective exacerbation of previously undiagnosed chronic obstructive pulmonary disease (COPD). Treatment involved bronchodilators, steroids and bilevel pressure support non- invasive ventilation.
One hour after NIV had been established, the patient’s respiratory acidosis was worse and his clinical picture was unchanged. He was intubated then transferred to Intensive Care. CTPA ruled out significant pulmonary emboli but was suggestive of pulmonary hypertension. Ventilation was not difficult, with near normal inspiratory pressures, and his minimal wheeze resolved quickly. As his respiratory acidosis normalised, his GCS rapidly improved to the point of safe extubation after just 48 hours. Given his obesity he was extubated to non-invasive pressure support ventilation immediately. After a further 24 hours, his gas exchange began to deteriorate again. Increasing inspiratory pressure improved his tidal volumes but his intrinsic rate of breathing slowed such that his minute ventilation remained static. He eventually found a stable equilibrium using nocturnal bilevel pressure support with a high mandatory backup rate (pressure control), which maintained a normal minute ventilation. Although he developed hypercapnoea each night, this was mild and eventually compensated. With the NIV, he did not obstruct, have hypopnoeic events or desaturated overnight, which markedly improved his daytime somnolence and effort of breathing.
What are the clinical features and approaches to management of obesity hypoventilation syndrome?