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ICU Fellowship Vivas – Type 1 Respiratory failure, Determination of Brain death and Failed intubation

Dr Swapnil Pawar January 3, 2023 293


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    ICU Fellowship Vivas – Type 1 Respiratory failure, Determination of Brain death and Failed intubation
    Dr Swapnil Pawar

 

Blog written by – Dr Madhuri Anupindi

 

  1. You are asked to review a 56F in recovery who became hypoxic post bronchoscopy. The bronchoscopy was done to investigate a 2 week history of increasing shortness of breath and bilateral infiltrates on CXR. She is intubated and ventilated with sats of 88% on an fio2 of 1. Her respiratory function tests from one week prior to admission show an FVC of 40% predicted and an FEV1 of 43% predicted with minimal bronchodilator reversibility, residual volume of 51% predicted, total lung capacity of 44% predicted, DLCO*corr of 16% predicted and DLCO/VA of 19% predicted. List the differential diagnosis of hypoxia post bronchoscopy in this patient.

Hypoxia may be secondary to complications from the bronchoscopy, complications from the anaesthetic/peri-procedural event, or an acute deterioration/progression in the underlying illness, causing her initial presentation on a background of severe restrictive lung disease.

Bronchoscopy related:

  • Atelectasis
  • Pulmonary haemorrhage
  • Pneumothorax
  • Bronchospasm

Anaesthetic/new pathology:

  • Anaphylaxis
  • Peri-procedural AMI
  • Pulmonary embolism
  • Aspiration

Worsening of underlying illness: recent lung function tests are consistent with interstitial lung disease, which can be secondary to numerous aetiologies.

  • Infective: viral, bacterial, fungal, parasitic à miliary TB, fungal infections
  • Cardiac: congestive cardiac failure à ischaemic, arrhythmia, valvular
  • Vascular: diffuse alveolar haemorrhage, vasculitis
  • Drug related: transfusion associated lung injury, amiodarone, eosinophilic pneumonitis, methotrexate, chemotherapy, azathioprine, bleomycin, cocaine, heroin, methadone, rituximab, sulfasalazine, anakinra, cyclophosphamide
  • Toxins: asbestos, silica, radiation, coal
  • Inflammatory/idiopathic: sarcoidosis, Wegener’s granulomatosis, polymyositis, idiopathic pulmonary fibrosis, cryptogenic organising pneumonia, amyloidosis
  • Autoimmune: HLH, rheumatoid arthritis, Goodpastures, SLE, scleroderma
  • Neoplasm: infiltrative neoplasm, lymphangitis carcinomatosis
  • Genetic: neurofibromatosis, Niemann-pick disease, Gaucher disease

What are findings on lung function tests consistent with this patient having interstitial lung disease?

  • Decreased FEV1 and FVC with a normal FEV1/FVC ratio
  • Decreased DLCO
  • Decreased total lung capacity

What is DLCO*corr?

This is the DLCO adjusted for haemoglobin. DLCO is the diffusing capacity for carbon monoxide which assesses the lungs ability to transfer gas from inspired air to the bloodstream. The DLCO is affected by factors that change the properties of the alveolar-capillary membrane and those that change haemoglobin and capillary blood volume.

Anaemia, decreases the blood’s carbon monoxide carrying capacity and thus decreases DLCO.

DLCO*corr, adjusts the  DLCO for the patient’s haemoglobin.

Outline your immediate management of this patient

Management: targeted initial assessment aimed at identifying and treating reversible causes and contributors of her hypoxia and consideration of appropriate disposition for this patient.

  • Targeted assessment to exclude and rapidly treat reversible causes
    • Brief history of anaesthetic and bronchoscopy details and findings
      • Grade of airway
      • Sats prior to starting and trajectory during the bronchoscopy
      • Medications given
      • Any pathological findings
      • Any difficulties ventilating, obvious bleeding
      • Haemodynamic issues
    • Reversible causes
      • ETT adequately positioned, not obstructed – suction catheter passing easily
      • Evaluate for pneumothorax: auscultate/CXR/bedside US à drain if present
      • Atelectasis: CXR à cautious PEEP increase depending on peak/plateau pressures aiming plateau pressures < 30 cm h20
      • Anaphylaxis: rash, bronchospasm à adrenaline
      • Bronchospasm: bronchodilators, steroids, sedate and paralyse, appropriate ventilator settings, IV magnesium, IV ketamine, adrenaline
      • Dysynchrony or inappropriate ventilator settings: sedate + paralyse patient, check ventilator settings I:E of 1:1, low tidal volumes 4-6ml/kg and higher respiratory rate given restrictive lung disease, pplat < 30cmh20
      • Ventilator malfunction: try BVM, change ventilator
      • Poor peripheral perfusion à unreliable sats trace, check ABG for gas exchange, pH and lactate
    • Disposition
      • Full monitoring, ensure adequate IV access
      • Transfer to ICU (may currently be on a transport ventilator and improve with standard ventilator
      • Art line, CVC, NGT and IDC insertion if not already done
      • Consideration of whether patient would be suitable VV-ECMO or lung transplant candidate if not improving à may need to transfer to more specialised centre if this is the case

Following acute assessment and treatment of identifiable reversible pathology:

  • Further evaluation
    • History: previous investigations including micro tests for bacteria/fungi/viruses/parasites, TTE to evaluate cardiac function, other organ function UEC/LFT, review previous imaging including CXR and CT scan if done, other co-morbidities (including malignancies, autoimmune conditions, genetic diseases or other conditions associated with ILD), previous medications and exposures (especially those associated with ILD), treatment given during this admission such as antimicrobials or steroids
    • Exam: top to toe
      • Autoimmune/vasculitis signs
      • Auscultation: creps/bronchial breath sounds
      • Calf swelling: DVT, tachycardia à PE
      • Signs of heart failure
      • Rash, lymphadenopathy, dry eyes, splenomegaly à sarcoidosis
    • Investigations
      • Bedside: ABG (gas exchange), TTE (cardiac function especially pulmonary hypertension, signs of right heart strain), ECG
      • Microbiology: ensure samples sent with bronch including MCS, AFB, fungal culture
      • Bloods: autoimmune markers/vasculitis (ANA, rheumatoid factor, anti-ccp, ANCA, anti-ds-DNA, antiphospholipid antibodies, myositis panel), UEC/LFT: organ function
      • Imaging: CXR, high resolution CT chest/CTPA if patient stable enough to transfer
      • Review BAL findings: can help to narrow down cause of lung disease
    • Management
      • Management of hypoxia
        • Supportive:
          • Sedate and paralyse à aim train of four of 0
          • Inhaled pulmonary vasodilators: use prostacyclin in our institute
          • Permissive hypercapnoea as long as pH > 7.2, aim pao2 > 60, ventilate 1:1 ratio, aim plateau pressure < 30cmh20
        • Specific: depends on cause and contributors, broad spectrum antimicrobials if concerns re infection and while waiting for investigation results, consider immunosuppression in conjunction with discussions with respiratory team and depending of results of investigations from admission
      • Supportive management
        • DVT prophylaxis, PPI, enteral nutrition
        • Update and discuss care with family
  1. 45M elective surgery 2 days ago for removal of an arachnoid cyst complicated by localised posterior fossa haemorrhage requiring emergency craniotomy and evacuation of the clot within 6 hours of the original surgery. Prior to emergency surgery he had fixed dilated pupils. Propofol and morphine have been off for 24 hours and on exam he has a GCS of 3, no cough or gag, and fixed dilated pupils. CT report prior to emergency craniotomy shows acute posterior fossa haemorrhage with brain stem compression and early cerebellar tonsillar herniation. What would be your approach to prognostication?

I am concerned that this patient has a very poor prognosis and is showing signs indicating loss of brainstem function. However, the underlying pathology may have only affected the brainstem and there may still be blood flow and function in the cerebral hemispheres. Therefore, he does not meet the preconditions for clinical exam alone to determine if death has occurred.

I would ensure that there are no other confounders present (check organ function – UEC/LFT/TFT/metabolic parameters such as BSL, check temperature, ensure not paralysed and has not been given other sedative medications which may be longer lasting such as thiopentone) and organise for a repeat CT scan to evaluate for potential reversible causes such as a new haemorrhage or hydrocephalus. If there were no reversible causes or confounders and he remained GCS 3 with no signs of brain stem function on clinical testing, I would then organise for a four vessel digital subtraction cerebral angiogram. This would all be done in collaboration with the treating neurosurgical team and with ongoing discussions with the family to provide updates and support.

What are the preconditions that must be met in order to determine death by clinical examination?

These are outlined in the ANZICS Statement on Death and Organ Donation.

Firstly, there must be clinical or neuroimaging evidence of sufficient intra-cranial pathology to deteriorate to permanent loss of all neurological function.

The patient must:

  • Meets period of observation: at least 4 hours of mechanical ventilation throughout which the patient has:
    • Been GCS 3
    • Had fixed dilated pupils
    • Had no cough/tracheal reflex
    • Had no spontaneous breaths
    • If the patient is post cardiorespiratory arrest/acute hypoxic-ischaemic encephalopathy or been hypothermic (< 35 degrees) for > 6 hours: there should be a waiting period of at least 24 hours after rewarming before determination of death by clinical exam alone
  • Meets preconditions
    • Temp ³ 35 degrees
    • Normotension SBP ³ 90 MAP ³ 60mmHg
    • Exclusion of effects of sedative medications
    • Absence of neuromuscular blocking drugs
    • Absence of severe metabolic, electrolyte or endocrine disturbances
      • Glucose 3 – 25
      • Sodium 125 – 160
      • Phosphate ³5
      • Magnesium ³5
      • Urea < 40
      • Severe hypothyroidism, hypoadrenalism
    • Absence of acute liver failure or decompensated chronic liver disease
    • Able to examine one ear and one eye
    • Able to assess the motor response in the facial nerve to painful stimulus in the upper limbs and to assess the motor response in the upper limbs to painful stimulus in trigeminal sensory region
    • Ability to perform apnoea testing

 

What would be consistent with the absence of brain perfusion on four-vessel angiography?

Absence of intra-arterial contrast above the level of the carotid siphon in the anterior circulation and above the foramen magnum in the posterior circulation. If this is required, it must still be preceded by the performance of the parts of the clinical examination possible in that patient.

What are the other options for demonstrating the absence of brain perfusion?

  • Intra-arterial catheter angiography with digital subtraction is the gold standard
  • Radionuclide imaging: technetium 99m radiolabelled hexamethyl propylene amine oxide (Tc-99m HMPAO) is a radionuclide that crosses the blood brain barrier and is retained by the brain parenchyma by conversion from a lipophilic to a hydrophilic form. The absence of this intra-cranially compared to its presence extra-cranially can be used to determine lack of brain perfusion
  • Computed tomography angiography: if DSA or radionuclide imaging is not readily available
    • If CTA is performed it is recommended that the four point scale is used which looks at enhancement of peripheral intracranial arteries at 20 seconds and central veins at 60 seconds after an IV injection of 120ml of >300mg/ml non ionic contrast injected at 3ml/sec via a power injector through an 18 gauge or bigger intravenous catheter
    • Absent brain perfusion is then demonstrated if there is
      • Absent enhancement of both middle cerebral artery cortical branches and
      • Absent enhancement of both internal cerebral veins
    • MRI and transcranial doppler are not currently acceptable techniques for neurological determination of death

 

If performing clinical brain death testing, what motor signs are compatible with permanent loss of brain function?

Spinal reflexes are compatible with permanent loss of brain function. These may include:

  • Deep tendon reflexes
  • Lazarus sign (bilateral arm flexion, shoulder adduction, hand raising to above the chest, potentially can also have flexion of trunk, hips and knees)
  • Extensor or flexor plantar response
  • Head turning
  • Undulating toe reflex (plantar flexion of big toe followed by sequential plantar flexion of 2nd – 5th toe)
  • Extension pronation movement of upper limbs or non specific flexion of lower limbs
  1. Teaching a skill station on the management of the difficult airway. An unexpected failed intubation in a hypoxic patient who is also difficult to ventilate with BVM. The patient has been given sedation and a non-depolarising neuromuscular blocker.

Equipment available: BVM, oropharyngeal and nasopharyngeal airways, ETT, LMAs, MAC blade, intubating bougie, intubating stylet, intubating LMA, video laryngoscope. Guide the junior registrar through appropriate steps following an unexpected failed intubation in a hypoxic patient who is known to be difficult to BVM ventilate.  

There are several difficult airway algorithms available.

Emphasise: main priority is OXYGENATION while planning and optimising for a definitive airway

  • Known difficult bag valve mask à Insert LMA (discuss with registrar types and sizes of LMAs)
    • If able to oxygenate and ventilate via LMA à would call for more assistance and optimise patient’s oxygenation
      • Explore reason for failed intubation: what was view, what blade was used, how was patient positioned, were any adjuncts used, how much paralysis was given, were there too many secretions
        • For ETT optimisation think of: manipulations of head/neck/larynx, changing blade, was ETT right size, do we need more suction, was muscle tone optimised?
      • If unable to oxygenate via LMA
        • Remove LMA and consider optimisation strategies for LMA
          • Different size/type of LMA, change inflation of LMA, give further sedation/paralysis
        • If still unable to oxygenate via LMA with new changes à remove LMA and go back to BVM and optimise
          • Ensure adequately sedated and paralysed
          • Place two nasopharyngeals and an oropharyngeal airway
          • Use 2 handed bagging technique

Once stable/rising sats then optimise again for intubation. Consider

  • Position: sniffing morning air position
  • Right blade: use video laryngoscope in this case as already failed intubation and can teach with same
  • Ensure adequately sedated and paralysed and suction secretions
  • Adjunct: can use bougie or stylet

Also, talk about essential non-technical skills like closed-loop communication, teamwork, role allocation etc.

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