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 66 year old woman was admitted to the ICU with acute type II respiratory failure secondary to a community acquired pneumonia (CURB-65 score 4) complicating severe COPD (FEV1 40% predicted). Collateral history revealed many concerning features; the patient had a poor exercise tolerance (mMRC dyspnoea scale score 3, exercise tolerance <100m), was alcohol dependent (drinking 120 units per week) and previously had been admitted to hospital with an exacerbation of COPD requiring NIV, and treatment for acute alcohol withdrawal.
Mechanical ventilation was commenced using a lung-protective strategy with permissive hypercapnia. Sedation was achieved using remifentanil and propofol, targeting a Richmond Agitation Scale Score (RASS) of -2 to 0. A noradrenaline infusion was commenced to maintain a mean arterial pressure of ≥65mmHg. A neutral cumulative fluid balance was targeted. Broad-spectrum antimicrobial therapy was continued as per local antimicrobial guidelines. Intravenous B vitamins were administered and enteral feeding was established via a nasogastric tube.
In view of the patient’s comparatively poor pre-morbid function and high risk of delirium, early extubation to NIV was identified as the preferred strategy. By day 3 the patient had improved such that this became a realistic goal. In order to prevent acute alcohol withdrawal, yet use benzodiazepines sparingly to avoid associated respiratory depression, remifentanil-propofol sedation was substituted for a clonidine infusion, which was continued following extubation. Low doses of chlordiazepoxide were used as rescue therapy in accordance with Clinical Institute Withdrawal Assessment for Alcohol scale (CIWA-Ar) scoring.
The patient progressed well, was weaned from both NIV and clonidine and was discharged from HDU to a respiratory ward on day 8. She survived to hospital discharge.
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A 35-year-old man was admitted through the Emergency Department with a three-day history of sore throat, drooling of saliva and fever. In the twenty-four hours leading up to his admission he had reported increasing difficulty breathing and hoarseness. His past medical history included obesity and non-insulin dependent diabetes mellitus.
On initial assessment he was found to be stridulous, drooling, tachypnoeic, tachycardic and febrile. Supplemental oxygen was applied and intravenous access obtained, with blood cultures being sent prior to administration of broad-spectrum antibiotics (Ceftriaxone, Benzylpenicillin and Metronidazole). Despite nebulised Adrenaline, intravenous fluid and intravenous dexamethasone, he continued to deteriorate and was transferred to the anaesthetic room for definitive airway management. Findings at intubation were consistent with acute epiglottitis. Swabs were taken and oral fibreoptic intubation was successfully performed.
Following admission to the ICU, he was mechanically ventilated and sedated with infusions of Propofol and Remifentanil. Antibiotic therapy was continued and he was commenced on regular dexamethasone to reduce epiglottic oedema. He required a low- dose noradrenaline infusion to maintain blood pressure, and was commenced on an insulin sliding scale. Two days after admission his airway was reassessed with direct laryngoscopy, and was found to be significantly less oedematous.
At this stage a sedation hold was performed, with the patient opening eyes spontaneously and seeming to obey commands. He was extubated to humidified facemask oxygen but shortly afterwards became agitated, combative and delirious (CAM-ICU positive). The patient was re-intubated within a two-hour period and Propofol and Remifentanil sedation was recommenced. Over the following two days, he remained inappropriate on daily sedation holds, and by this stage was receiving bolus doses of Haloperidol for episodes of acute agitation. CT imaging of his brain revealed no abnormality, and lumbar puncture was negative for central nervous system infection. Intravenous dexamethasone had been weaned, in view of the improvement in epiglotittis seen at laryngoscopy.
By day six of his admission he remained neurologically inappropriate on sedation hold, and was changed to an intravenous infusion of Dexmedetomidine at 0.7 mcg/kg/hr. Remifentanil was weaned off at this time, and Propofol infusion was reduced to baseline levels. This continued for a further twenty-four hours, by which time he was neurologically appropriate on sedation hold, obeying commands, and was extubated uneventfully.
On direct questioning, the patient did not recall his first extubation episode on Intensive Care. He did recall a combination of vivid visual and auditory hallucations, including the presence of insects in his bed, hearing persecutory voices and a feeling of helplessness and fear. He made a full recovery, and these symptoms had fully resolved by the time he was discharged from hospital.
What is the role of dexmedetomidine in the prevention and management of ICU delirium?
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 20 year-old man was admitted to his local district hospital with a severe head injury following an assault. On arrival in the Emergency Department he was agitated with a reduced conscious level, with evidence of blunt trauma to the head and neck. Prior to intubation, his Glasgow Coma Score (GCS) was recorded as 7 (E1V2M4), and with cervical spine precautions he underwent intubation with subsequent mechanical ventilation and sedation.
An urgent CT brain and cervical spine revealed early evidence of intracerebral contusions with diffuse areas of petechial intracerebral haemorrhage identified. Nasal and maxillary fractures were also seen, with no cervical spine pathology identified. He was transferred to the regional neurological centre for assessment and ongoing management.
On arrival in the Neurosurgical Intensive Care unit the patient underwent insertion of an intracranial pressure monitor revealing an intracranial pressure (ICP) of between 30-35 mmHg. Pupil reactivity was sluggish bilaterally. Sedation was changed to infusions of propofol, fentanyl and midazolam, positioning was optimised with 20 degree head-up tilt, endotracheal tube ties were replaced and targeted mechanical ventilation to EtCO2 4- 4.5kPa. Central venous access was established and an infusion of Noradrenaline was used to target cerebral perfusion pressure to 70mmHg.
Initial medical management stabilised ICP below 25mmHg, but within the next 12 hours this began to rise despite neuromuscular blockade and infusion of hypertonic saline. Further CT imaging revealed progression of the intracerebral contusions with developing oedema. The patient was transferred to the operating theatre for insertion of an external ventricular drain. CSF drainage resulted in an immediate but small improvement in ICP but again over the next 12 hours it began to rise, and decision was made for bifrontal decompressive craniectomy.
Subsequent recovery was slow and was complicated by ventilator-associated pneumonia, a protracted tracheostomy wean and severe agitation. The patient underwent intensive neuro-rehabilitation and had been decannulated, but was left with persistent cognitive impairment, seizures and depression.
What is the rationale for performing decompressive craniotomy in TBI?
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.
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A 70-year-old lady was admitted to the Intensive Care Unit (ICU) with respiratory failure and septic shock secondary to pneumococcal pneumonia. She developed multi- organ failure, requiring a prolonged period of mechanical ventilation and weaning, and also developed acute kidney injury requiring haemofiltration. Once a tracheostomy was performed and sedative infusions weaned, she was noted to be acutely delirious. Her sleep pattern was severely disrupted, with extended periods of nighttime wakefulness and sleep fragmentation, increased daytime sleep and difficulty with sleep initiation requiring pharmacological intervention.
Following exclusion of organic causes including CT brain imaging, the delirium was managed with a combination of antipsychotic medications including haloperidol, mirtazapine and quetiapine. Benzodiazepine-based night sedation was used but found to be ineffective in establishing sustained sleep.
A trial of night sedation with infusion of Propofol did not have any ongoing or long-lasting benefit other than the immediate sedative effects and providing control of agitation. A trial of Dexmedetomidine infusion also yielded similar results, although a more sustained daytime anxiolytic effect was noted. Benzodiazepine therapy was changed to supplementation of Melatonin. At around this time, the delirium began to resolve and the patient was able to more actively engage in physiotherapy and patient care. By the time of ICU discharge over thirty days later, and following successful weaning and decannulation, the patient’s sleep pattern had improved significantly.
What are the implications of sleep deprivation in the critically ill patient and how can it be managed?
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 »
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.
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?