ICU Fellowship Vivas – Pregnancy with Asthma, ICH and Pancreatitis with Respiratory Failure

Written by – Dr Madhuri Anupindi

1. 32F: 28 weeks pregnant with a background of asthma. She has been in hospital for 4 days for the management of hypertension and has become acutely breathless. What are the main differential diagnoses?

Differentials:

• Related to pregnancy:
  • Pulmonary oedema secondary to pre-eclampsia
  • Pulmonary embolism (pro-coagulant state)
  • Aspiration (decreased oesophageal sphincter tone)
  • Metabolic acidosis e.g. due to acute fatty liver of pregnancy, renal failure
• Exacerbation of chronic conditions
  • Acute exacerbation of asthma – pneumothorax
  • Pre-existing respiratory or cardiac disease (unlikely)
• New acute pathology
  • Drug related: allergic reaction, TRALI,
  • Sepsis with ARDS, pneumonia
  • Pain from another pathology
• Iatrogenic
  • Excess IV fluids
  • Magnesium toxicity

How would you further assess to identify the cause of her deterioration?

This would involve targeted history, examination and investigations.

• History
  • Prior to hospital admission: Co-morbidities, asthma control (hospitalisations, preventers, steroids, ICU admissions, recent spirometry/lung function tests), regular meds, allergies, smoking
  • Trajectory in hospital: meds for hypertension, end organ function, recent bloods
  • Acute deterioration: associated symptoms, similar episodes, timeline, meds given
• Exam:
  • ABCS: vitals, signs of anaphylaxis, auscultation ?wheeze or creps, haemodynamic status
  • Targeted systems:
    • Neuro: mentation, weakness + reflexes (hyporeflexic and weak in Mg toxicity)
    • Sepsis: fevers
    • Calf pain/swelling
    • Abdominal tenderness
  • Investigations
    • Bedside:
      • ABG/VBG: gas exchange, metabolic status, BSL, lactate
      • CTG: baby wellbeing
      • ECG: right heart strain, tachycardia, acute ischaemic changes
      • UA: protein, signs of infection
    • Bloods
      • UEC/CMP: renal function, mag level
      • FBC: hb level (bleeding), platelets (low in HELLP), leucocytosis (but often physiological in pregnancy)
      • LFT: liver function tests (can be affected in pre-eclampsia)
      • Consider septic screen, haemolysis screen, troponin depending on patient
    • Imaging
      • Consider lung US, CXR, VQ, CTPA

What are the considerations of managing asthma in pregnancy?

Prevention/minimisation of asthma exacerbations is essential

• Asthma is the most common chronic disease to affect pregnant women
• Poorly controlled asthma and asthma exacerbations increase the risk of poor outcome for fetus. Therefore the goals of asthma management during pregnancy are to maintain the best possible control and prevent exacerbations.
• Ensure adequate inhaler technique
• Avoid exposure to cigarette smoke, allergens
• Treat rhinitis, GORD
• Regular monitoring and follow up

Approach to asthma control:

• Stepwise approach to treatment (risks of treatment are much less than the risks of acute exacerbations)
  • Short-acting beta-agonists as relievers
  • Add regular inhaled corticosteroids or inhaled corticosteroid/long-acting beta-agonist combination
  • Regular daily ICS-LABA maintenance plus low dose reliever + SABA reliever as needed
  • Regular daily medium/high dose ICS-LABA + low dose reliever/SABA reliever as required
  • Short course oral corticosteroids
  • Consider long-acting muscarinic antagonist

Management of acute exacerbations:

• Assessment:
  • Peak flow meter: normal values of peak expiratory flow are not significantly altered by pregnancy
  • ABG/VBG: will have a compensated respiratory alkalosis in pregnancy  paco2 usually 30 with hco3 of 20 – therefore a ‘normal co2’ may actually be a sign of severe compromise in the pregnant patient
  • Fetal monitoring: CTG
• General:
  • Avoid maternal hypoxia (will thus help avoid fetal hypoxia)  use supplemental oxygen and have continuous sats monitoring aiming sats ³ 95%
  • Avoid supine position (aortocaval compression by gravid uterus)
  • Generally lower threshold for ICU admission
  • Consider NIV if severe (but also risk of gastric distension/aspiration)
  • If requiring intubation  often difficult intubation due to airway oedema, decreased FRC and increased oxygen consumption (quicker desaturation), breast tissue, increased risk of aspiration
• Medications: same as for non-pregnant
  • Beta agonists – salbutamol
    • Inhaled (no evidence that inhaled beta agonists interfere with uterine contactions)
    • Parenteral beta agonists rarely needed
  • Muscarinic antagonists – ipratropium
  • Corticosteroids (generally oral or IV if acute exacerbation)
  • Intravenous magnesium sulfate if severe
  • Consider ketamine if severe

2. 62M: admitted to ICU 10 days ago with acute pancreatitis, not tolerated enteral feeding. BG: 30 pack year smoker, ETOH 4 – 8std/day. Intubated and ventilated for 6 days with worsening gas exchange. What are your differential diagnoses for the deterioration in his gas exchange?

Complications related to:

• Acute pancreatitis
  • Cardiac: SIRS associated cardiomyopathy, SIRS response with capillary leak
  • Resp: ARDS, pleural effusion, pulmonary oedema, chylothorax
  • GIT: pancreatic ascites, abdominal compartment syndrome, ileus, pancreatic necrosis
  • Renal: acute renal failure
• ICU stay
  • Fluid overload
  • Infection
  • Pneumothorax
  • Atelectasis
  • PE
  • New pathology such as AMI
  • Delirium/agitation – biting on tube, dysynchrony, non-compliant with physio
• Exacerbations of chronic conditions
  • Exacerbation of COPD
  • Alcohol withdrawal
  • Decompensated liver failure
  • Exacerbation of cardiac failure

How would you assess him?

Assessment:

• History
  • Chronic conditions, COPD control, alcoholic cardiomyopathy
  • Medications: diuretics, inhalers, steroids
  • Trajectory in ICU: reason for intubation, fluid balance, recent vitals trends including fevers, investigations performed – organ function and trend, recent micro, recent imaging complications from his pancreatitis (e.g. infections)
• Exam
  • Vital signs: etco2 and trace, secretions
  • Sedation/paralysis, neurological function
  • Level of respiratory support on ventilator
  • Auscultation
  • Abdominal exam, drains, IAP
  • Fluid status, urine output
• Investigations
  • Bedside: ECG, UA, TTE, ABG
  • Bloods: septic screen, biochem, inflammatory markers, organ function
  • Imaging: CXR, CTCAP

How would you measure his intra-abdominal pressure?

Measurement:

• End expiration in supine position, abdominal muscle contractions absent (ideally patient paralysed), transducer zeroed at iliac crest in mid axillary line
• Connect non compressible tubing and transducer to indwelling IDC, bladder emptied and clamped, 25ml saline introduced into bladder, reading obtained after 1 minute to allow detrusor to relax
• Confounders:
  • Patient related: increased pelvic pressure, high detrusor tone or fibrosis, incomplete paralysis, pelvic haematoma, chronic cystitis with small contracted bladder
  • Measurement related: leaking transducer system, improper set up or calibration

What is abdominal compartment syndrome?

Abdominal compartment syndrome is a sustained intra-abdominal pressure > 20mmHg (with or without an abdominal perfusion pressure < 60mmHg) that is associated with new organ dysfunction/failure. It can be primary (originating from abdominal pathology), or secondary (originating from extra-abdominal pathology).

Risk factors for ACS include:

• Intra-abdominal pathology: infection, trauma, massive haemorrhage, retroperitoneal haematoma, ascites, ileus, acute pancreatitis, abdominal wall burns
• Treatment related: laparoscopy with excessive pressures, peritoneal dialysis, massive transfusion, massive fluid resuscitation, mechanical ventilation, prone positioning
• Other: high BMI, sepsis

What are the consequences of ACS?

• Respiratory
  • Decreased compliance, increased peak airway pressures  hypercapnoea
  • Increased intrapulmonary shunt and VQ mismatch
  • Atelectasis and pneumonia
• CVS
  • Decreased preload  hypotension – due to decreased venous return from venous compression and raised intrathoracic pressure
  • Increased afterload  increased compression of arterial vessels in abdomen and PVR due to raised intra-thoracic pressure
  • Decreased RV output due to raised intrathoracic pressure, raised PVR
  • Increased CVP and LVEDP, reduced compliance due to elevation of diaphragm displacing heart and increased afterload
• CNS
  • Increased ICP
• Renal
  • Failure
• GIT
  • Mesenteric ischaemia
  • Decreased intestinal mucosal perfusion
  • Bacterial translocation
  • Portal vein thrombosis
  • Decreased lactate clearance
  • Ileus
  • Decreased gastric emptying, feed intolerance, aspiration
• Haem
  • Lower limb venous thrombosis

Briefly outline the management principles of abdominal compartment syndrome?

• Improve abdominal wall compliance
  • Sedation and analgesia
  • Paralysis
  • Avoid head of bed > 30 degrees
• Evacuate intra-luminal contents
  • NG decompression
  • Rectal decompression
  • Prokinetics
• Evacuate abdominal fluid collections
  • Paracentesis
  • Percutaneous drainage
• Correct positive fluid balance
  • Avoid excess fluids
  • Diuretics
  • Colloids/hypertonic fluids
  • Haemodialysis
• Organ support
  • Optimise ventilation
  • Titrate PEEP
  • Maintain APP > 60mmHg
• Surgical decompression
  • Temporary abdominal closure

3. 70F in ED who has presented with altered conscious state and L sided weakness. Intubated, BP 240/120mmHg. BG: IHD and AF. A CT scan demonstrated a large R sided tempero-parietal ICH with IV extension. What are your initial management priorities?

Management priorities:

• Quick assessment including targeted history, exam and investigations
  • Targeted history:
    • Presentation: any trauma, vomiting, seizures, syncope
    • Co-morbidities:
      • AF: ?on anticoagulation that needs to be reversed
      • IHD: ?on antiplatelets
      • Known intra-cranial pathology ?malignancy
      • Baseline function
      • Known hypertension and control
    • Medications including antiplatelet/anticoagulants, allergies
  • Exam: GCS, pupils, signs of other trauma from fall
  • Ix:
    • Bedside: ECG (arrhythmias), BSL, VBG/ABG for gas exchange/quick electrolytes
    • Bloods: FBC (platelets/Hb), coags, consider ROTEM, group and hold (may need transfusion/surgery)
    • Imaging: CXR for tube/NG position, consider CTA if suspicion of underlying vascular lesion, may need MRI at some point if concerns regarding underlying mass
  • Management
    • Logistics:
      • Adequate monitoring and access
      • Bed in neurosurgical ICU or transfer to a neurosurgical unit
    • Specific
      • BP control: short-acting, IV agents hydralazine aim SBP of approximately 140mmHg
      • Neurosurgical input re-EVD or evacuation of haematoma
      • Neuroprotective measures: BSL 6 – 10, normoxia, normocapnia, avoid fever
      • Reversal of anticoagulation if present
    • Supportive
      • Correct position of ETT
      • Analgesia/sedation for ETT
      • Organ support: lung protective
      • Social support: discuss with family

What is the evidence for acute blood pressure management in haemorrhagic stroke?

Parameters for blood pressure control in acute haemorrhagic stroke is controversial. Australian Clinical Guidelines recommend that the target systolic blood pressure may be acutely reduced to around 140mmHg but not much more in those with intracerebral haemorrhage, but acknowledge that this is based on weak evidence. The NICE UK guidelines recommend aiming for a SBP of below 140mmHg within 2 hours of starting treatment and maintaining this for at least 7 days in patients who present within 6 hours of symptoms and have a SBP of 150 – 220mmHg, and to consider achieving these targets in a more controlled fashion in those with a SBP > 220mmHg. The American Heart Association recommends targeting a SBP of < 140mmHg in those with an initial SBP of 150 – 220mmHg.

The 2 main trials focusing on acute BP control in acute haemorrhagic stroke are ATACH-2 from 2016 and INTERACT 2 from 2015.

ATACH-2 was an RCT that compared rapid lowering of SBP to 110 -139mmHg versus 140 -179mmHg in hypertensive adults with acute ICH. It found there was no difference in modified Rankin score of 4- 6 at 3 months and no significant difference in other secondary outcomes except for a higher incidence of renal adverse events within 7 days in the intensive treatment arm.

INTERACT 2 compared intensive BP lowering of < 140mmHg to < 180Mg and found that there was no difference in death or severe disability between the groups. Ordinal analysis of modified Rankin scores indicated improved functional outcomes with intensive BP management with the best outcomes for SBP 130 – 139mmHg over 24 hours.

Currently, there is no firm consensus on the optimal BP targets and they need to be individualised for the patient. Currently, there is weak evidence that a BP target of around 140mmHg is generally safe. There is some signal that recurrent excessive BP fluctuations may also predict poor clinical outcomes, so close monitoring of blood pressure is essential.