A 50-year-old man was brought to the emergency department. He had sustained a burn affecting 55% of his total body surface area and a significant inhalational injury. In the emergency department he was intubated and ventilated, central venous, arterial and urinary catheters were placed and resuscitation begun using the Parkland formula.
He was transferred to burns intensive care. Fluid resuscitation was continued using Hartmann’s solution. A bronchoscopy was performed; 1.26% sodium bicarbonate was used for lavage. He became increasingly tachycardic and hypotensive. He was oliguric. His haematocrit was 0.45. Fluid status was difficult to assess clinically; he felt warm to touch. An oesophageal Doppler probe was sited which demonstrated low stroke volume and corrected flow time. His Doppler parameters improved with each 250ml bolus of Hartmann’s solution but the effect was short lived. Noradrenaline and then adrenaline infusions were used in an attempt to maintain blood pressure. After a significant volume of crystalloid had been given, approximately 12 hours after the time of injury, 4.5% human albumin solution was requested. This seemed to have a more prolonged effect than Hartmann’s solution. Over the next 12 hours the patient’s haemodynamic status stabilised and he was able to undergo initial surgical management of his burn 36 hours after presentation.
What is the evidence for the use of human albumin solution for fluid resuscitation in critically ill patients.Read More »
A 52 year old female was admitted to the ICU with septic shock secondary to cholangitis. She had liver cirrhosis secondary to alcoholic liver disease, although she had been abstinent since an admission with acute alcoholic hepatitis 2 years previously. She had recently entered the assessment pathway for orthotopic liver transplantation.
She presented to the Emergency Department with a short history of fever and confusion and falls. She was pyrexial, tachycardic and hypotensive. Her inflammatory markers were elevated and her liver enzyme profile suggested cholestasis. There were no other localising features on examination or preliminary investigation.
She was commenced in the ED on broad-spectrum antibiotic therapy (piperacillin-tazobactam) and fluid resuscitation consisting of Hartmann’s solution and 4% human albumin solution. Her blood pressure remained labile throughout the early part of her admission. She fulfilled the criteria for septic shock with evidence of evolving multi-organ dysfunction.
The patient received early, aggressive multi-organ support. Tracheal intubation and pressure-controlled ventilation were instituted due to grade III/ IV encephalopathy and a high work of breathing in response to profound metabolic acidaemia. A thorough clinical assessment of intravascular volume status was conducted, suggesting that the patient was adequately filled. Vasopressor therapy was initiated using noradrenaline to achieve a target MAP of 65mmHg. CVVHDF was commenced to control the severe acidaemia and hyperlactataemia.
The patient was vasoplegic and remained profoundly hypotensive despite rapidly escalating doses of noradrenaline and the addition of hydrocortisone. Continued assessment of intravascular status confirmed adequate filling and cardiac output monitoring using a pulse-contour analysis system confirmed a low SVRI- high cardiac output state. Her noradrenaline requirements soon exceeded 0.4mcg/kg/min-1, at this point a vasopressin infusion was introduced at 0.03units/hr-1. This was associated with an improvement in haemodynamic indices; the target MAP was achieved and thereafter remained stable with a slow reduction in noradrenaline requirement. On day 2 the continuous vasopressin infusion was converted to terlipressin by bolus dose regime (2mg QDS).
An urgent ultrasound scan of her biliary system revealed an obstructed common bile duct which was treated by percutaneous biliary drainage. An Enterococcus was isolated from drain fluid and blood cultures within 48 hours and antibiotic therapy tailored accordingly. The patient was weaned from organ support and discharged to the hepatology unit 9 days after admission.
What is the rationale for the use of vasopressin in septic shock? Are vasopressin analogues as effective?Read More »
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 68 year-old gentleman was admitted to the Emergency Department in cardiac arrest. He had complained of sudden onset upper abdominal pain to his wife immediately prior to a collapse, and bystander cardiopulmonary resuscitation (CPR) was commenced whilst emergency services were called. He had a background of ischaemic heart disease, insulin-dependent diabetes, peripheral vascular disease and hypertension.
On arrival, the Paramedic crew found him to be in ventricular fibrillation was the predominant rhythm. Despite appropriate advanced life support with defibrillation and administration of adrenaline and amiodarone over multiple cycles. His airway was supported with an I-Gel supraglottic airway device, and he was transferred to hospital urgently.
Ischaemic heart disease is the leading cause of death in the world, and sudden cardiac arrest is responsible for more than 60% of adult deaths from coronary heart disease. Early and effective CPR, early defibrillation and physiological support post-resuscitation form the chain of survival .
Assessment of the patient’s airway on arrival in the Emergency Department revealed evidence of vomit in the pharynx, and endotracheal intubation was performed. Vomitus was aspirated from his endotracheal tube, indicating pulmonary aspiration either at the time of collapse or during the resuscitation attempts. Sidestream capnography was connected to a self-inflating bag administering high-concentration oxygen. The initial capnography indicated a flattened end tidal carbon dioxide (EtCO2) trace with a highest partial pressure of 1.5 kPa. Chest auscultation was performed and air entry was confirmed as being equal bilaterally.
Chest compressions continued uninterrupted and by this stage the overall resuscitation attempt had been ongoing for 45 minutes. The rhythm had changed to pulseless electrical activity, and despite effective CPR, administration of adrenaline and fluids, there was no return of spontaneous circulation (ROSC). Blood gas analysis revealed a severe metabolic acidosis (pH 6.8, lactate 15.2 mmol/L) and by this stage the highest EtCO2 recorded was 0.9 kPa. Following discussion with the team, and on the grounds of futility, the resuscitation attempt was abandoned.
What is the role of capnography in cardiac arrest?
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 female presented with acute kidney injury and sepsis. She required fluid resuscitation, haemofiltration and cardiovascular support for 2 days, following which she was discharged to the renal ward for on-going haemodialysis. She underwent dialysis every 2-3 days for the next 3 weeks. Whilst on the ward she deteriorated acutely one evening, developing respiratory distress, followed by a respiratory arrest. She was intubated and ventilated transferred to the critical care unit.
A CTPA was negative for pulmonary embolus, but showed large bilateral pleural effusions. Tracheal suctioning was initially clear but later copious blood stained secretions were removed. A bedside cardiac echo performed by the consultant intensivist showed a globally sluggish left ventricle, which was overfilled, and the inferior vena cava measured 3cm also suggesting fluid overload. A trial of furosemide failed and she was aggressively haemofiltered to remove the excess fluid. Troponin was only mildly raised, and not thought to be suggestive of an acute cardiac event. She was extubated 24 hours later, but had two further episodes of flash pulmonary oedema requiring non-invasive ventilatory support whilst haemofiltration was re-commenced for fluid balance reasons. In total twelve litres of fluid were removed, with significant improvement in the patient’s condition. Repeat echocardiography prior to discharge showed an improving left ventricular function and IVC measurement of 2cm with greatly increased compliance.
What is the evidence that focussed echocardiography helps guide decision-making in intensive care?Read More »
A middle-aged man underwent an elective re-do aortic arch replacement for a 6.1cm ascending aortic aneurysm distal to a pre-existing composite graft. Past medical history included a Bentall procedure (metallic aortic valve replacement, aortic root and ascending aorta replacement with coronary re-implantation into the composite graft) 20 years ago. Preoperative echocardiogram showed a well seated AVR and good biventricular function. Drug history included Warfarin (target INR 2-3) and Atenolol.
Anaesthetic induction and re-sternotomy were uneventful. Cerebral oximetry (rSO2) monitoring was utilized in this case. Cardiopulmonary bypass (CPB) was achieved uneventfully and deep hypothermic circulatory arrest (DHCA) was instituted. The patient was cooled to 18°C using CPB and icepacks. Prior to CPB and DHCA being commenced, intravenous thiopentone and methylprednisolone were administered for neuroprotection. Total DHCA time was 40 minutes and selective anterograde perfusion via the right axillary artery (chosen as it is relatively free of atheroma) was employed when rSO2 dropped to <40% and they remained >40% for the remainder of DHCA. Total CPB time was 105 minutes.
Following successful insertion of a new graft, the patient was carefully rewarmed to normothermia and weaned off CPB uneventfully, only requiring minimal vasopressor support. The patient was transferred to the cardiothoracic critical care unit.
After optimization of cardiorespiratory physiology, correcting coagulopathy and maintaining normothermia, with strict avoidance of hyperthermia, the patient was extubated the following day. For the first 48-72 hours postoperatively, delirium was the most active medical issues and this was managed according to conventional treatment. There was no focal upper or lower limb neurology. The patient did not require any other organ system support.
Following resolution of his delirium the patient was discharged to the ward to continue his rehabilitation. Prior to discharge, at approximately postoperative days 7-10, he was complaining of loss of short-term memory, reduced attention span and difficulty with finding words. A neurology review attributed this to cognitive dysfunction but no formal tests were carried out. A neurology clinic follow-up and an outpatient MRI scan were arranged.
What are the neurological complications after cardiac surgery?Read More »
An elderly woman woke from sleep with acute breathlessness and wheeze. She had been treated for late-onset asthma by her GP. She had no other previous medical history and was exceptionally active. In the emergency department she received standard treatment for acute severe asthma . A systolic murmur was noted and an echocardiogram requested. After 24 hours of relative stability she experienced a sudden deterioration in her breathing and despite increased therapy for her asthma she had a respiratory arrest.
Following resuscitation and emergency tracheal intubation she was transferred to the ICU. On examination she was peripherally cool. Chest auscultation revealed extensive wheeze and crackles. Investigations revealed a raised troponin I (0.92 ug/L) and raised BNP (530 pmol/L). Her CXR revealed pulmonary oedema and her ECG showed sinus rhythm without overt evidence of ischaemia.
Initial problems included poor oxygenation, oliguria and a low cardiac output state (LiDCO revealed cardiac index of 2.1 l/min/m2). She received norepinephrine (up to 0.6 mcg/kg/min) and dobutamine (up to 40 mcg/kg/min). Levosimendan was introduced to augment her cardiac function as her CI had not achieved to 2.5l/min/m2. Norepinephrine was increased to maintain a MAP over 65mmHg. After levosimendan her urine output, acid-base status and CI were not substantially improved. The dobutamine had been stopped and she remained on norepinephrine.
An echocardiogram revealed hyperdynamic LV and RV and mitral regurgitation, which was initially assessed as being moderate in severity. Cardiac surgical opinion was that the risk of mitral valve surgery was unacceptably high.
Over the following few days she had problems with recurrent compromising atrial fibrillation and was treated with varying degrees of success with a variety of measures including DC cardioversion, amiodarone, metoprolol, digoxin and verapamil. Diuresis was obtained with a frusemide infusion and ramipril was introduced. Her CXR appearances improved and ventilation became easier.
On the 3rd day a trans-oesphageal echocardiogram confirmed severe mitral regurgitation (MR) with prolapse of the posterior mitral valve (MV) leaflet due to a ruptured chordae tendinae. There was resultant left atrial enlargement and pulmonary hypertension with an estimated PA systolic pressure of 60-70mmHg. Within a week she was weaned from ventilatory support and recovered sufficiently to mobilise independently prior to discharge home.Read More »