Category: Domain 3

Disease Management

Decompressive Craniotomy in Traumatic Brain Injury

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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?

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Mechanical Ventilation of Chronic Obstructive Airways Disease

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A 68-year-old went into respiratory arrest on the chest ward. He had been admitted 2 weeks previously for an exacerbation of chronic obstructive airways disease (COAD). He has had two previous episodes of reduced conscious level due to hypercapnoea, which resolved with non-invasive ventilation and oxygen titration.

He was immediately intubated on the ward and transferred to the intensive care unit for ventilation. Hypoxia was corrected to a PaO2 >8.0kPa with a moderate FiO2. However he remained very difficult to ventilate and maintained a persistently high PaCO2. The highest level was 21kPa. He was treated with B2 agonist nebulisers, anti-muscarinic nebulisers, systemic steroids, aminophylline infusions, magnesium infusions and a ketamine infusion. He also needed vasopressor support and for a period of time continuous renal replacement therapy. After a week when his ventilator pressures reduced he had an uneventful percutaneous tracheostomy. Sedation was then reduced and he was awake and spontaneously breathing but with a high level of support. He was recurrently troubled by episodes of bronchospasm and air trapping. The lowest settings for inspiratory pressure were 14 cmH2O. He deteriorated a number of times before care was withdrawn and he died 20 days later.

Can we predict which COAD patients will benefit from mechanical ventilation?

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Intra-Aortic Balloon Pump for Cardiogenic Shock

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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 »

Sleep Deprivation on the ICU

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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?

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ICP Monitoring and Acute Liver Failure

ICP Monitoring and Acute Liver Failure

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A 28-year-old lady presented to the medical team jaundiced with cramping upper abdominal pain and multiple episodes of vomiting over the previous day. She admitted ingesting Paracetamol 8 grams 3 days previously (staggered throughout the day) ostensibly to treat a frontal headache. She had been commenced on Citalopram 1 week previously for depression but denied taking any intentional overdose. On examination, she was slightly drowsy but GCS 15. HR 109, BP 136/92. Sats 98%on air. Her chest was clear, she was warm peripherally but jaundiced with some epigastric and RUQ tenderness on palpation. Her urine output was 10-20ml/hr.

Full Blood Count revealed Hb 152, WCC 24.7, Plats 301. She was in acute liver failure with Bil 189, AST 22970, ALT 13040, ALP 426 and coagulopathic with PT 82, APTT 72, Fib 0.7 Urea 5.7, Cr 193. Paracetamol and Salicylate were not detected. She was not acidotic with H+ 35, OCI2 3.7, pO2 17, Bic 20, BE –3. Lactate 7.1.

She was commenced on N-acetylcysteine and transferred to Critical Care. She was reviewed by the Hepatobiliary surgical team and placed on the super-urgent list for liver transplant. 

On Day 2, she became encephalopathic with GCS E3M5V5 and she was intubated and ventilated.Her PT had increased to 168 (INR >15) and she became anuric. She commenced FFP and Cryoprecipitate transfusions that improved her PT to 17, APTT 34 and Fibrinogen 1.5. An Intracranial Pressure (ICP) monitor was inserted and an opening pressure of 19mmHg was found. 2 hours post-insertion, it was noticed that her right pupil had increased in size from 2mm to 4mm and was poorly reactive. ICP remained at 16 and pCO2 4.1.

A brain CT showed a large haematoma in the right frontal region around the ICP bolt (which was not in the brain parenchyma but sitting in the skull) and mass effect with 5mm midline shift. There was also some lack of grey-white matter differentiation and sulcal effacement in keeping with diffuse oedema and mass effect.

INR was 1.7 and so further FFP was given. She was discussed with the neurosurgical registrar (in a separate hospital) who advised they would not drain at present but he would discuss with his Consultant and call back. 

Soon after, her right pupil increased to 8mm and the left to 7mm. Repeat CT brain showed slightly increased right frontal haematoma with 6mm midline shift and global oedematous cortical changes but no herniation. The ICP readings were thought to be inaccurate due to proximal placement and she was medically treated for raised ICP with hypertonic saline, mannitol and then therapeutic hypothermia. Despite this treatment, her pupils were fixed and dilated and so a thiopentone infusion was commenced.

The neurosurgeons advised that they would insert a further ICP monitor when INR <1.3 and so further FFP was given. An ICP bolt was inserted and the opening pressure was >120.

Discussions between the ICU, hepatobiliary and neurosurgical teams confirmed that she had a non-survivable injury and so this was discussed with her family. She was rewarmed, paralysis and then sedation were discontinued, brain stem death testing took place and she was extubated in the presence of her family. She died on Day 3 and was referred to the Coroner for further investigation.

What is the rationale for measuring ICP in acute liver failure?

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Management of Refractory Intracranial Hypertension

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A young man with no significant past medical history was admitted to the Emergency Department following an assault. His Glasgow Coma Score on arrival was 8 with a motor score of 4 and there was evidence of an external head injury. Pupils were symmetrically reactive. He was intubated to facilitate further management. Both primary and secondary surveys were unremarkable apart from multiple contusions to the face and scalp. Multi-slice CT showed no intrabdominal or intrathoracic injury but significant intracranial pathology with subarachnoid and intraventricular blood and multiple, principally frontal contusions. No associated neuraxial fracture was seen.

Urgent neurosurgical opinion was sought which confirmed no immediate target for surgical intervention. The patient was transferred to the intensive care unit where appropriate monitoring was established including the insertion of a fibreoptic subdural intracranial pressure bolt. Initial intracranial pressure was measured at 18 mmHg. Sedation with propofol and alfentanil infusions was titrated to a RASS score of -3, ventilation adjusted to a PaO2 > 13 kPa and PaCO2 4.5-5.0 kPa as per the Brain Trauma Foundation guidelines and an infusion of noradrenaline started to achieve a cerebral perfusion pressure of 60 mmHg. The patient was nursed 30° head-up and although active cooling was not undertaken, temperature maintained at less 35-37.5°C.

There was initial stability but approximately 24 hours after admission sustained rises in intracranial pressure (ICP) in excess of 25 mmHg were seen, necessitating boluses of sedation, the addition of atracurium by infusion, administration of hypertonic saline, cooling to 35°C and brief periods of hyperventilation to a PaCO2 4.0-4.5 kPa albeit without significant control. Urgent repeat CT brain was undertaken which showed evolution of the contusions with signifiant oedema and loss of both the lateral ventricles and basal cisterns.

On further consultation, neurosurgical colleagues again felt that no immediate surgical option was viable; in particular that attempts to insert and external ventricular drain were unlikely to be successful and that contusionectomy would produce significant disability. The patient was randomised into the RESCUEicp trial and thiopentone infusion started at a rate to produce isoelectrical activity on three lead electroencephalogram.

What are the management options for refractory intracranial hypertension?
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Post Operative Cognitive Deficit after Cardiac Surgery

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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 »

Acute Mitral Valve Failure

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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 »

Arthrogryposis & Paediatric Difficult Airway

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EMERGENCY MANAGMENT OF A DIFFICULT AIRWAY IN AN INFANT WITH ARTHROGRYPOSIS MULTIPLEX CONGENITA

A 4 month old infant with arthropgryposis multiplex congenital was admitted to the paediatric assessment unit. The infant had been acutely unwell over the preceding 12 hours with respiratory compromise and a productive cough with green sputum. He had signs of respiratory distress with a RR of 40, pulse oximetry showed SpO2 of 85% on air and only 90% with a facemask, reservoir bag and high flow oxygen. It was felt that the infant would need to be intubated and ventilated. Two months before the infant had had a respiratory arrest on the neonatal ward and was unable to be intubated. That situation was resolved by mask ventilation and rescue with an LMA. There were obvious concerns that direct laryngoscopy would be unsuccessful and may precipitate a terminal decline in the patient’s condition.

The infant’s breathing was supported by bag/mask ventilation whilst he was transferred to an ENT theatre. Further anaesthetic support and an ENT surgeon were sought. I.v. access was established through a scalp vein. Ventilation was switched to an Ayres T piece with Jackson-Rees modification. Induction of anaesthesia was initiated with sevoflurane and oxygen. Direct laryngoscopy showed a Lehane and Cormack grade 4 view.

A rigid bronchoscope with video camera monitor was used by the ENT surgeon to obtain a view of the glottis. An epidural catheter was placed down the side port of the bronchoscope and was directed through the vocal cords. The bronchoscope was removed and a fine bore suction catheter was railroaded over the epidural catheter to give more stiffness. The positions of the end of the catheters were checked with the bronchoscope. A size 3.0cm uncuffed endotracheal tube was then railroaded over the catheters into trachea. Position and length were confirmed with the bronchoscope and ventilation was continued. The arrangement is shown in Figure 1.

The child was then transferred to the adult ICU where a retrieval team arrived to transfer the patient to a PICU.

What is arthrogryposis? Describe some methods for achieving control of the difficult paediatric airway.Read More »

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 »