Category: 3.6

Recognises and manages the patient with neurological impairment

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 »

Refractory Status Epilepticus

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A middle aged man presented with seizures. For 4 days he had been feeling unwell with coryzal symptoms, frontal headache and dizziness. He had ‘not been himself’ for some months. He had no previous medical history and had never had a seizure before. The ambulance crew noted that he was confused and witnessed a generalised tonic-clonic seizure. On arrival in hospital he was severely agitated and uncooperative and received IV lorazepam.

He was not adequately protecting his airway, saturations were 100% on high flow oxygen, temperature was 37.8, his pulse was 88, BP 129/90mmHg, blood sugar was 7.7. Clinical examination did not reveal any abnormality except for diminished level of consciousness. A presumptive diagnosis of meningitis / encephalitis was made. His trachea was intubated, he received fluids, parenteral vitamins, IV ceftriaxone and acyclovir. A CT head (with contrast) was obtained and a lumbar puncture were normal. His blood tests, CXR, urinary toxicology screen, and ECG were non-contributory. Arterial blood gas analysis revealed changes consistent with being post ictal and then (whilst ventilated) normalised.

His sedation was weaned and once extubated he remained very drowsy, even 18 hours after his last sedation. A Glasgow Coma Score (GCS) was recorded at E1V1M5 (7/15). His pupils were equal and reactive, and he was moving all 4 limbs. Both plantar responses were down-going, and tone and reflexes were symmetrical. He had myoclonic jerking of his left hand but no rhythmical muscle activity was evident. To protect his airway he required reintubation of his trachea and re-institution of ventilation.

In addition to sedation with propofol and alfentanil he received therapeutic phenytoin. An electroencephalogram (EEG) performed on his second day, off sedation, revealed continuous periodic sharp and slow wave complexes at around 1Hz with intermittent high amplitude waves in the left temporal region and bursts of rhythmical activity in the right temporal region. At the time of the EEG he had some abnormal motor activity – continuous movement of his fingers and twitching of an eyelid and rhythmical jerking of both of his arms. An MRI of his brain was normal.

In this clinical context the EEG was interpreted as being consistent with encephalitis and non-convulsive status epilepticus.  Phenobarbitone was started in addition to the phenytoin. Normothermia and normoglycemia was maintained. To improve the management of his non convulsive status we continuously monitored his cerebral electrical activity with a bispectral index (BIS) monitor and bitemporal EEGs. We targeted a burst suppression of 20-50%. Propofol was ineffective at reducing the BIS without causing limiting hypotension but midazolam was effective.

Further investigations did not further our search for the primary diagnosis. A further EEG was performed 24 hours later, off midazolam but whilst on 350mg/hr of propofol. He developed some rhythmical motor activity and his EEG revealed ongoing abnormal electric activity, consistent with continued non-convulsive status, which resolved in response to a bolus of propofol. A possible diagnosis of limbic encephalitis was considered and methylprednisolone (1g IV) was administered.

A repeat MRI showed increased abnormal signal changes in the amygdala and hippocampus, which is supportive of the diagnosis of limbic encephalitis.

Despite optimal medical treatment his EEG showed more severe and continued abnormal electrical activity. Thiopentone was added to his anti-seizure regime. By the 19th day from initial presentation multiorgan failure had developed. He required ventilation with high airway pressures and high inspired oxygen concentrations for lung injury due to ventilator associated pneumonia, vasoactive drugs to support his cardiovascular system through the associated sepsis, haemofiltration for renal failure and had ileus with failure of enteral feeding. There were still signs of seizure activity despite concurrent administration of propofol, midazolam, phenytoin, levetiracetam, phenobarbitone and sodium valproate. Supportive treatment was withdrawn following diagnosis of brain-stem death. His family did not permit a post mortem examination.Read More »

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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Steroids in Cervical Spine Injury

Steroids in Cervical Spine Injury

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A previously fit and well 46 year-old was admitted via the emergency department having sustained a neck injury whilst horse riding. She was unable to move her arms and legs immediately after the fall. On arrival to the Emergency Department, she was alert and orientated. Examination of the cardiovascular and respiratory system was unremarkable although there was evidence of diaphragmatic breathing.

Examination of her neurological system revealed:

•A sensory level at C6
•Absent upper limb reflexes except for brisk bicep reflex bilaterally
•⅖ power in shoulder abductors bilaterally
•Flaccid paralysis of her lower limbs
•No anal tone

She was initially managed in a hard neck collar with full spinal immobilisation. CT brain was reported to be normal. CT neck showed an obviously displaced fracture of C5 and C6 vertebral bodies. She was transferred to the intensive care unit for cardiovascular, respiratory and neurological monitoring while a definitive treatment plan was being considered. After discussions with the orthopaedic surgeons, it was decided not to commence high-dose steroids. This decision was reinforced after discussion with the local neurosurgical and spinal units. It was also decided not to surgically stabilise the c-spine due to the higher risk of respiratory complications. She was transferred to the spinal rehabilitation unit after 2 days.

What is the role of steroids in cervical spine injury?Read More »

Ethylene Glycol Poisoning

Ethylene Glycol Poisoning

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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 »

Coiling versus Clipping Subarachnoid Haemorrhages

Coiling versus Clipping Subarachnoid Haemorrhages

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A 40 year old female presented with a severe sudden onset headache, and deteriorated in the emergency department with worsening agitation and confusion requiring intubation and ventilation for her own safety. A CT scan diagnosed a Fisher Grade 4 subarachnoid haemorrhage and obstructive hydrocephalus. Clinical presentation was scored as Hunt and Hess grade 4 or World Federation of Neurosurgeons grade 4. The patient was transferred to the local tertiary Neurocritical care unit where an extra-ventricular drain was inserted overnight. The following day the patient underwent coiling of her right middle cerebral artery aneurysm in the radiology suite. A Magnesium infusion and Nimodipine therapy were commenced to reduce the risk of vasospasm. On initial sedation hold she woke up agitated so she had an early tracheostomy placed to allow controlled wake up. She had a straightforward respiratory wean from the ventilator over the next few days. Neurological recovery was good (Glasgow coma score improved to 14/15) and the patient was discharged to the ward for on-going neuro rehabilitation and repatriation to the base hospital.

What are the risks of clipping vs coiling subarachnoid haemorrhages?Read More »

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 »

Neuroprognostication Post Cardiac Arrest (Post TTM Era)

Neuroprognostication Post Cardiac Arrest (Post TTM Era)

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A  young adult female with known diagnosis of poorly controlled type 1 diabetes mellitus was admitted with out-of-hospital cardiac arrest. She had only recently been discharged from hospital after an admission with diabetic ketoacidosis. On arrival she had a GCS 3 with minimal respiratory effort. She was in profound DKA. Her temperature was 34.7°C on admission to ICU and she had targeted temperature management aiming for 36°C which was achieved within 2 hours. Her pH had normalised to 7.35 within 8 hours. 48 hours later one pupil became fixed and dilated. CT brain was consistent with global hypoxic ischaemic injury. EEG and SSEP on day 3 revealed severe lack of normal cortical activity. After discussion with family, treatment was withdrawn on day 4.

How do we undertake neuroprognostication after cardiac arrest in the post-TTM era?

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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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Intensive Care Acquired Weakness

Intensive Care Acquired Weakness

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A cardiovascularly fit 65 year old man was admitted with septic shock secondary to community acquired pneumonia, which progressed to multi-organ failure. During his recovery it was noted that he had generalised weakness with no focal neurology. He underwent respiratory weaning, and rehabilitation therapy over the next 4 weeks but had persistent weakness at his ICU discharge.

How can ICU-acquired weakness be diagnosed and managed?Read More »