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ICU Fellowship Vivas – Delayed Cerebral Ischemia, Hepatic Encephalopathy and Burns

Dr Swapnil Pawar July 10, 2022 136


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    ICU Fellowship Vivas – Delayed Cerebral Ischemia, Hepatic Encephalopathy and Burns
    Dr Swapnil Pawar

Blog Written by Dr Madhuri Anupindi

 

  1. A phone call from registrar overnight (have not previously worked with). 36F who has been in ICU for 5 days. She was admitted with a SAH, WFNS grade 3 from a right MCA aneurysm. She underwent emergency coiling. She has been extubated for 24 hours and has an EVD set to drain at 10cmH20. Her GCS has been 10 – 12 until tonight when she was noted to not be herself for 1 – 2 hours. She is now drowsy and is becoming difficult to rouse. What is your response?

There are both logistic and clinical aspects.

I am concerned that this patient has had a deterioration in her neurological function either secondary to a complication of her SAH (re-bleeding, hydrocephalus, haematoma, vasospasm, seizures) or due to a new pathology. My response would involve communicating these concerns to the registrar and advising them about the important aspects in assessing and stabilising this patient.

Logistic issues:

  • Given that I have not worked with the registrar previously and unsure of their level of seniority, I would want to provide extra support by coming into hospital to help assist in the management
  • Notify the neurosurgical team and prepare for CT scan (transport monitor, access, radiology informed)

Initial assessment and stabilisation. I would advise the registrar to:

  • Rapidly assess the patient’s vital signs and neurology
    • Assess saturations, protection of airway and difficulty of airway
      • Provide supplemental oxygen, assess aspiration risk  airway manoeuvres if not maintaining. If no anaesthetic experience or concerns re difficulty call anaesthetic team
    • Assess HR/BP  haemodynamic support if required, aim SBP 120 – 150mmHg at present as aneurysm secured
    • Assess neurology: what is the exact GCS breakdown, are there any focal deficits, what is the ICP, how much has the EVD been draining/is it blocked, any blood in EVD, any signs of seizures
      • If EVD not draining: assess that EVD not clamped, no kinks, that it is oscillating and ICP has normal waveform  if all is good then lower drain and observe for CSF dripping
      • Signs of seizures: IV benzos: midazolam 0.1mg/kg, IV levetiracetam loading 20mg/kg
      • If delayed cerebral ischaemia: SBP 140 – 160mmHg (however exclude other causes)
      • Ventriculitis: CSF WCC/RCC ratio
    • Assess for other contributors/causes of decreased LOC
      • Recent medications given
      • Metabolic changes: ABG, BSL, electrolytes, renal, hepatic function
      • Fevers/sepsis

The patient goes for an urgent CTB which shows no new acute pathology and is thought to have delayed cerebral ischaemia. What is delayed cerebral ischaemia and what are the risk factors?

Delayed cerebral ischaemia is the development of a new focal neurological deficit or a decrease of at least 2 points on the Glasgow Coma Scale which lasts more than 1 hour, was not apparent immediately after aneurysm occlusion, and cannot be attributed to other causes. DCI is traditionally thought to be secondary to vasospasm, however now more recent studies postulate that radiological vasospasm may be associative rather than causative, and that the aetiology may be multifactorial.

Risk factors for DCI include:

  • SAH factors
    • Higher radiological grade
    • Higher clinical grade
  • Patient factors:
    • Smoking
    • Female
    • Diabetes
    • Younger age
    • Hypertension
    • Hyperglycaemia
    • Cocaine use

Briefly list the management options for delayed cerebral ischaemia?

 Management aims to prevent or minimise any further neurological injury.

Pharmacological therapy:

  • Nimodipine: mainly preventative

Haemodynamic optimisation

  • Vasopressors titrated to a higher blood pressure: in our unit 140 – 160mmHg  regular monitoring of patient’s neurology and may then adjust BP targets depending on neurological response
  • Aim euvolemia

Endovascular therapy:

  • Balloon angioplasty
  • Intra-arterial milrinone or verapamil

 

  1. 27M (80kg) found after an explosion in his garage. In ED GCS 8 (E2V2M4), sats 88% on 15L o2, RR 40, HR 123, BP 88/45 and significant burns to his face, chest and limbs. Describe your assessment and management priorities specific to the burn injury.

Assessment and management involve trauma team activation, targeted history, primary and secondary survey as per ATLS guidelines. From a burns perspective, specific attention needs to be paid to early securing of his airway, management of his hypoxic respiratory failure, adequate fluid resuscitation and haemodynamic support, adequate analgesia, and evaluation of the extent and appropriate management of his burns.

Logistics:

  • Activate trauma team and burns team
  • Full monitoring on patient but may be limited by extent of burns (especially ECG monitoring)
  • Will need admission to ICU eventually: may be via OT depending on findings on assessment  if this is not a burns centre will need retrieval organised to nearest burns centre

Targeted history:

  • Patient related: allergies, medications, co-morbidities, last ate/drank
  • Trauma related: events surrounding explosion in garage, observations on the scene, timing of injury, evidence of drug/alcohol ingestion
  • Treatment prior to arrival: any first aid to burns such as burns placed under water, analgesia, amount of IVF given

Primary survey

Airway/C spine control

  • Urgent securing of airway given hypoxic resp failure and facial burns (warning signs singed nasal hair, hoarse voice, stridor, facial burns, soot in sputum). May be a difficult intubation so requires anaesthetics/ENT input.
  • Video laryngoscope, inline stabilisation due to C spine concerns, RSI, pre-oxgenate
  • Insert NGT
  • C spine precautions  may be difficult if facial/neck burns – ideally once intubated for sandbags

Hypoxic respiratory failure

  • Assess and treat contributors to the hypoxic respiratory failure: restrictive burns around the chest may require escharotomies, exam and CXR for sequelae from trauma such as pneumothoraces may need chest drains, ABG for carbon monoxide/methaemoglobin levels and lactate as well as adequacy of ventilation, consider cyanide toxicity
  • Lung protective ventilation aim pPlat < 30cmh20, titrate o2 to sats ³ 92% unless evidence of carbon monoxide poisoning or methaemoglobinemia

Circulation and haemodynamic support:

  • IV access through intact skin, full bloods including G+H as may need transfusion/OT, FBC to assess haemoconcentration, UEC/LFT for organ function and AKI, CK for evidence of rhabdomyolysis, BSL due to low GCS, consider other blood tests such as troponin if evidence of sternal fractures/blast injury/cardiogenic shock, alcohol level/paracetamol level if concerns about co-ingestants
  • Assess extent of burns: TBSA – and for any ocular/airway involvement
  • Fluid resuscitation: modified Parklands: 3ml/kg x TBSA (first 50% in 8 hours then remaining in 16 hours)  crystalloid to begin with but avoid large volumes of normal saline, ensure fluids are on a warmer
  • IDC to monitor fluid balance and aim 0.5ml/kg/hr urine output
  • Assess and treat contributors to hypotension: sequelae of trauma such as a blast injury or bleeding, or secondary to burns such as large fluid shifts or cyanide toxicity.

Burns management:

  • Wound management: clingfilm, dressings, burns team involvement re debridement
  • Assess for complications: escharotomies if circumferential burns and close neurovascular observation, assess for rhabdomyolysis, consider antimicrobials if wounds significantly contaminated
  • ADT
  • High risk of losing heat: ensure warmed room, warmed fluids/blood products if given, minimise exposure, bair hugger if required
  • Assess for complications from burns: escharotomies if circumferential, rhabdomyolysis
  • Adequate analgesia: boluses of opiate initially, regular paracetamol (if no overdose) and then infusion of opiate once intubated
  • Will need an NGT as will eventually require feeding as hypercatabolic

Other aspects:

  • Assess for other injuries and assess for focal neurological deficits
  • Will likely need CT pan scan once stable due to mechanism of injury
  • Secondary survey

List the methods available to estimate the extent of his burns?

There are several methods available:

  • Lund and Browder Chart:
    • Most accurate method as it compensates for variation in body shape with age
  • Palmar surface method:
    • Surface area of the patient’s palm including fingers is equal to 1% TBSA
    • More accurate for smaller burns
  • Wallace rule of 9s:
    • Body is divided into areas of 9% e.g. 9% each arm, 18% each leg.
    • This method is faster and more convenient but is not accurate in children or obese people

 Briefly outline the evidence for colloid versus crystalloid fluids in burns resuscitation

Colloids are sometimes recommended as part of fluid resuscitation in burns patients due to the proposed physiological rationale of being able to act as a plasma expander, be a fluid sparing agent and counteract hypoalbuminemia. There is a paucity of high quality evidence about the utility of albumin in burns fluid resuscitation. A meta analysis in 2014 of both randomised and non randomised clinical trials found that albumin was found to be associated with a lower incidence of compartment syndrome and mortality. However, the authors acknowledged significant weaknesses in the available evidence, with a lack of randomised studies and many retrospective trials included.

 

  1. 45M admitted with UGI bleed and undergoes endoscopy and banding of oesophageal varices. His GCS at presentation was 15. Over the next 24 hours he has a progressive decrease in conscious level. You are called by the new medical consultant who suspects the patient has hepatic encephalopathy and wants him admitted to ICU. How would you assess the patient to determine the cause of the altered LOC?

There are many potential causes for this gentleman’s deterioration in conscious state including complications of his initial procedure such further GI bleeding or delirium, complications secondary to his hepatic dysfunction such as coagulopathy with an ICH, or new pathology such a septic encephalopathy. Many of these pathologies can also result in hepatic encephalopathy. Assessment would involve targeted history, examination and investigations.

History

  • Co-morbidities:
    • Hepatic dysfunction including information about the extent (e.g. Childs Pugh class or MELD score, synthetic dysfunction), underlying cause of liver disease and previous complications such as previous hepatic encephalopathy
    • Other co-morbidities such as renal failure, thyroid/adrenal/pituitary disease, autoimmune conditions which can result in decreased level of consciousness
  • Medications/toxins: normal medications at home (?withdrawal or missing appropriate meds), new medications given (?adverse reactions , interactions or accumulation secondary to organ dysfunction), alcohol and drug use (potential withdrawal states)
  • Allergies
  • Trajectory in hospital: duration of admission, localising symptoms (e.g. infections), fevers, vital signs, falls, bowel habits, recent blood tests and organ function, endoscopic report

Exam:

  • Vital signs, fever, sats
  • Neurological:
    • Level of consciousness
    • Signs of raised ICP: papilloedema
    • Any focal deficits
    • Hepatic encephalopathy: asterixis, dysarthria, nystagmus, hyperreflexia, delirium, clonus
  • Signs of chronic liver disease: muscle wasting, jaundice, ascites, palmar erythema, spider naevi
  • Signs of other pathology: infection, trauma, endocrinopathies, autoimmune conditions

Investigations:

  • Bedside: ECG, UA (infection), CXR (infection/aspiration), ABG/VBG: (gas exchange, lactate, glucose)
  • Bloods: FBC (Hb for UGI bleed, platelet for synthetic function, WCC and differential for infection), UEC (AKI, raised urea out of proportion of creatinine may suggest further UGI bleed), LFTs (hepatic function), coags (?coagulopathy), ammonia (useful as a trend), blood cultures if concerns re sepsis
  • Imaging: potentially CXR if concerns on respiratory exam, CTB for ICH
  • Other: consider LP, EEG depending on findings, ascitic tap if concerns re SBP

What are the potential precipitants of hepatic encephalopathy? 

Hepatic encephalopathy describes a spectrum of potentially reversible neuropsychiatric abnormalities that can occur in patients with liver disease and/or portosystemic shunting. Potential precipitants include:

  • Infection: any source, can include SBP
  • Drugs: narcotics, alcohol, benzodiazepines, non-compliance or accidental missing of medications such as lactulose
  • Metabolic: metabolic alkalosis, electrolyte disturbances such as hypokalemia, renal failure, hypoglycaemia, hypoxia, excessive intake of protein
  • Vascular: GI bleeding, hepatic or portal vein thrombosis, hypovolemia of any cause such as secondary to vomiting, diuretics, large volume paracentesis, portosystemic shunting such as post TIPS procedure
  • Other: hepatocellular carcinoma, constipation

Briefly outline the role of ammonia measurement in the diagnosis of hepatic encephalopathy

The diagnosis of hepatic encephalopathy is clinical and involves a focused history, examination and investigations to detect the characteristic neurological changes of hepatic encephalopathy, identify potential precipitants and to exclude other causes of deterioration. The role of ammonia measurement in the diagnosis of hepatic encephalopathy remains controversial. While ammonia is the best known neurotoxin that precipitates hepatic encephalopathy, it is not specific for hepatic encephalopathy, is not required for the diagnosis and its level does not correlate with clinical severity. Furthermore, its measurement can be confounded by sample error (requires sample to be placed on ice) and can be elevated in various non-hepatic conditions such as certain inborn errors of metabolism, with drugs such as valproate, and malignancies such as myeloma. Ammonia measurement is relatively simple, non-invasive and may help add support to a diagnosis of hepatic encephalopathy but patients can have hepatic encephalopathy with normal ammonia levels and conversely can have elevated ammonia levels with no clinical signs or symptoms of encephalopathy. tA retrospective review of 1200 patients with cirrhosis and a diagnosis of hepatic encephalopathy found that there was no correlation between lactulose dose and ammonia level and that ammonia measurement did not affect any patient centred outcomes. In summary, ammonia measurement has very little role in the diagnosis of hepatic encephalopathy with its measurement most likely just confirming your existing clinical findings and diagnosis.

After review you agree that this patient has hepatic encephalopathy. What factors would make you admit him to the ICU for ongoing management?

Patient related:

  • Need for ICU level support:
    • Haemodynamic compromise requiring vasopressors (e.g. secondary to sepsis or worsening hepatic failure)
    • Requirement for intubation (e.g. may have worsening GCS, have aspirated causing hypoxic respiratory failure)
    • Worsening end organ function e.g. hepatorenal syndrome needing CRRT
  • Need for closer observation
    • Deteriorating trajectory requiring more frequent observations
  • Presence of advanced care directive or other co-morbidities that would make ICU admission unsuitable: less likely in a 45 year old

Logistics:

  • Staffing related
    • Need for regular treatment such as hourly lactulose which may not be able to be facilitated on the ward
  • Hospital related
    • Ability of the ward or a higher level unit to provide closer observations, more intensive treatment without ICU admission

Outline your specific management of his hepatic encephalopathy.

 Specific management would involve identification and treatment of precipitating factors, ammonia lowering therapy and supportive therapy including nutritional support.

Identify/treat precipitating factors:

  • Aim euvolemia, avoid dehydration
  • Treat GI bleed: endoscopy, transfusion, PPI
  • Correct electrolytes and metabolic disturbances especially hypokalaemia, hypoglycaemia
  • Treat infection: antimicrobials, source control
  • Rationalise medications: cease hepatotoxins/potential contributing agents

Ammonia lowering therapy:

  • Lactulose: titrate to bowel habits, aiming 2-3 soft stools per day, can give orally if able to swallow or NGT can safely be inserted, otherwise can give PR
  • Rifaximin 550mg BD PO

Supportive management:

  • Nutritional support: thiamine and multivitamin, high fibre diet, dietician review, may need NG feeds depending on level of consciousness
  • Close monitoring and support of organ function: may need intubation if severe encephalopathy, monitor urine output/renal function – may need norad + terlipressin + conc albumin if hepatorenal syndrome suspected,
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