ICU Fellowship Vivas – Fluid resuscitation in Sepsis, Renal replacement therapy in AKI and PCV

Written by Dr Madhuri Anupindi

1. You are called to the Emergency Department to review a 50 year old male who was brought in by ambulance with a systolic blood pressure of 65mmHg. He is confused and his heart rate is 130 beats per minute. What are the sources of an inaccurate manual blood pressure reading?

• Patient related
  • Profound hypo or hypertension
  • Arrhythmias especially AF or tachyarrhythmias or severe bradyarrhythmias
  • Morbid obesity or cachexia
  • Full bladder
  • Recent activity/exercise
  • Agitation or stress
  • Subclavian stenosis/peripheral vascular disease
• Measurement related
  • Inappropriate cuff size
    • Too large: falsely low, too small: falsely high
  • Patient position: arm lower than the level of the heart, BP can be elevated
  • Fast deflation rate
  • Placing over clothing
  • Inappropriate cuff placement: bladder should be midline over the brachial artery, with the lower end of the cuff 2-3cm above the antecubital fossa

A radial arterial line is inserted in ED. The nurse notes that there is a significant difference between the arterial line and NIBP reading. List the potential causes for a difference in these readings?

• Error in invasive arterial measurement
  • Issues with the radial artery: stenosis, hypothermia, spasm or vasoconstriction, subclavian stenosis
  • Issues with circuit: arterial line or tubing kinked or clots or air bubbles present, loose connections, excessive amounts of tubing, pressure bag not inflated
  • Error in zeroing
  • Arterial line not levelled appropriately (should be at the phlebostatic axis)
  • Calibration error
• Error in NIBP measurement (due to factors mentioned above)
• Differences between sites (if arterial line and NIBP cuff are on different limbs)
  • Localised peripheral vascular disease/pathology
  • Aortic aneurysm or AAA

The patient still has a systolic blood pressure of 75mmHg and MAP of 50mmHg despite 2L of IV crystalloid. What further information would you use to decide whether to give him more IV fluid?

The cause of this gentlemen’s hypotension is unclear at present. This is important as my likelihood of giving further fluid rather than starting a vasopressor or inotropic agent, would also depend on the cause of his shock (earlier in cardiogenic or septic shock). In order to ascertain whether further IV fluid would be beneficial, I would want to obtain more information in order to elucidate the cause of his shock and his co-morbidities. This would involve obtaining historical, physical and investigative information.

Historical:

• Associated symptoms:
  • Hypovolemic shock: severe diarrhoea/vomiting, trauma, haematemesis/PR bleeding, ongoing thirst
  • Cardiogenic: chest pain, palpitations, shortness of breath
  • Obstructive: calf pain, shortness of breath, trauma, recent surgery, immobilisation
  • Distributive: fevers, infective symptoms, urticaria, recent potential allergen
• Co-morbidities
  • Ability to tolerate further IV fluid: renal failure on fluid restriction, history of cardiac failure/APO
  • Baseline BP: history of hypertension or hypotension, endocrinopathies (adrenal or thyroid dysfunction) normal meds (including anti-hypertensives, steroids)

Examination findings:

• Assessing risks/benefits of further fluid
  • Signs of hypovolemia
  • Signs of fluid overload
  • Signs of decreased end organ perfusion: confusion, decreased urine output
  • Multi-modal assessment of fluid responsiveness: passive leg raise, pulse pressure variation (acknowledging limitations but arterial line already in situ)
• Signs of cause of shock
  • Haemorrhage
  • Sepsis: localised signs of infection, fever, vasodilatation,
  • Anaphylaxis: urticaria, vasodilatation, angioedema
  • Signs of adrenal or thyroid disease
  • Cardiogenic: cool peripheries, prolonged cap refill, signs of chronic heart disease, signs of left/right heart failure
  • PE: tachycardia, increased work of breathing, desaturation, signs of right heart failure, calf swelling
  • Tamponade or tension: less likely unless recent trauma/surgery
  • Neurogenic: weakness, paralysis

Investigation findings:

• Signs of impaired end organ perfusion: raised lactate, acidosis, acute renal impairment
• Signs of cause of deterioration:
  • Bloods: raised inflammatory markers/WCC, raised troponin, deranged LFTs or UECs, raised lipase,
  • Bedside: ischaemic changes, arrhythmia or right heart strain on ECG, ketones or signs of infection on UA, TTE: regional wall motion abnormalities, LV or RV dysfunction, RV dilatation, tamponade, IVC size and respiratory variation
  • Imaging: infection/pneumothorax/APO on CXR, consider further imaging depending on other findings

 

Ultimately, if I did give him further IV fluid, I would re-assess his haemodynamics and clinical status after the bolus, to see if there was any improvement in parameters such as his MAP, HR, mental status, urine output and lactate.

Briefly outline the current evidence for use of restrictive fluid strategies in the management of patients with septic shock.

The amount and type of fluid to give patients with septic shock remains a contentious issue. The Surviving Sepsis Guidelines from 2021 recommend a volume of at least 30ml/kg of crystalloid given within the first 3 hours of resuscitation, but the quality of the evidence to support this is very low. A meta-analysis of 9 trials (total 637 adults with septic shock) published in CHEST in 2018 found no difference in all-cause mortality between lower and higher quantities of IV fluid resuscitation but the quality of the evidence was also very low.

The CLASSIC trial (NEJM 2022) was an RCT of 1554 adults with septic shock who were randomised to a restrictive group (IV fluid given for severe hypoperfusion or to correct overt losses) versus standard care (no upper limit for use of fluid). They found no difference in 90 day mortality or serious adverse events. Weaknesses of the study include that it was unblended, was powered for a large mortality reduction and there was a significant number of protocol violations. The CLOVERS trial (NEJM 2023) was an RCT of 1563 adults with hypotension secondary to suspected or confirmed infection and also compared a restrictive vs liberal fluid strategy. They also found no significant difference in 90 day mortality or secondary outcomes. Weaknesses include that it was unblinded, ran in one country and did not enrol a large number of patients who were otherwise eligible.

 

2. A 72M was admitted to ICU 5 days ago following primary resection and anastamosis of a perforated sigmoid diverticulum. He has a stable vasoactive agent requirement and is receiving empiric antibiotics. Over the last 12 hours he has produced a total of 200ml of urine and his creatinine has doubled from baseline to 300micromol/L. What is your differential diagnosis for the oliguria?

This gentleman currently has oliguric acute kidney injury (AKIN or KDIGO stage 2 or RIFLE stage injury) which may be secondary to multiple causes including; pre-existing pathology, secondary to his acute presentation, and secondary to issues during his ICU stay.

Pre-existing pathology:

• Diabetes
• Hypertension
• Nephrotoxins e.g. ACEI (cause efferent arteriolar dilatation), NSAIDs (inhibits prostaglandins which act as vasodilators that improve renal perfusion, also cause interstitial nephritis)
• Underlying renal impairment (had some degree as baseline creat 150), renal artery stenosis
• Underlying vasculitis/autoimmune disease

Secondary to his acute presentation and trajectory in ICU which may be pre-renal, renal or post-renal:

• Pre-renal
  • Hypotension: septic – perforated diverticulum, hypovolemic, myocardial event (ischaemia, septic cardiomyopathy, arrhythmias)
  • Cardiogenic
  • Abdominal compartment syndrome
  • Injury during surgery: renal artery
• Renal
  • ATN: secondary to vancomycin, aminoglycosides, contrast or sepsis, rhabdomyolysis
  • Interstitial nephritis: secondary to penicillins
  • Thrombotic microangiopathy secondary to DIC
• Post-renal
  • Ureteric or bladder injury during surgery
  • Blocked IDC

 

What would your management specific to his renal failure involve?

Management would consist of evaluation of the causes/contributors to his deteriorating renal function, supportive management to optimise his renal function and treatment of specific underlying pathology.

Evaluation

• History:
  • Past: co-morbidities, medications, baseline function, nephrotoxins, allergies
  • Presenting complaint and trajectory
    • Hypotension, sepsis, vasopressor support
    • Fluid input/output
    • Operative details
    • Antibiotics used, contrast
    • Urine output trend
  • Exam:
    • Shock: HR, BP, vasopressors, CVP, fluid status, signs of bleeding, fevers
    • Abdomen: ?ileus, distended, IAP
    • Genitourinary: IDC not blocked  flush same, urine colour
    • Compartments
  • Investigations:
    • Bedside: ECG (hyperkalemia), ABG (metabolic acidosis, lactate, electrolytes), bladder scan (IDC not blocked),
    • Bloods: UEC, DIC screen if relevant, CK, septic screen
      • Urea/creatinine ratio (> 100:1 pre-renal, normal renal)
    • Urine: microscopy  casts (epithelial casts if ATN), red blood cells (glomerular disease), eosinophils (acute interstitial nephritis), WCC (UTI), urinary myoglobin (rhabdomyolysis), urine osmol and sodium
      • Can do a fractional excretion of sodium (urine sodium/serum sodium / urine creatinine/serum creatinine) x 100
        • <1% pre-renal > 2% ATN
      • Consider renal US/CTKUB to evaluate for anatomical causes

Management

• Treat life-threatening pathology
  • Hyperkalaemia
• Optimise renal function
  • Avoid nephrotoxins, renally dose adjust medications
  • Adequate fluid balance
  • Dialyse if indicated
• Treat specific pathology
  • Pre-renal: fluids, haemodynamics, treat cause
  • Renal: stop contributing drugs
  • Post-renal: relieve obstruction
• Monitoring
  • Hourly urine output measurement
  • At least daily UECs to track renal function  may do more frequently if rapidly worsening or issues with hyperkalaemia
  • If persistent or requiring dialysis consider renal input – especially if going to transition to IHD or getting ready for ward so as followed up appropriately

 

What factors would influence your decision as to whether to start renal replacement in this patient?

The optimal timing of RRT initiation in the ICU remains controversial. I would consider a number of clinical factors prior to starting RRT.

Current clinical condition:

• Hyperkalaemia worsening or not responsive to medical management
• Significant fluid overload not responsive to medical therapy or deleteriously impacting on his oxygenation/ventilation or preventing extubation (if still intubated)
• Significant acidosis – vasopressor requirement is currently stable but if this was increasing or if metabolic acidosis was resulting in worsening respiratory status (in attempt to compensate) may consider earlier CRRT
• Confusion/decreased LOC with uraemia – especially if impacting on ability to extubate patient, patient’s participation in chest physio, patient compliance etc

Expected trajectory and baseline renal function:

• Rapidly deteriorating renal function

Suitability of patient for RRT

• Co-morbidities
• Functional status
• Advanced care directive

 

3. Describe the principles of Pressure Control Ventilation

Form of mandatory invasive ventilation where ‘pressure’ is the target variable that is set and the inspiratory pressure is maintained during the inspiratory phase. The inspiratory pressure is constant, therefore the flow (which depends on the pressure difference between the ventilator and the alveoli) diminishes over time. The initiation and termination of a pressure controlled breath depends on the rate and inspiratory time set on the ventilator

Settings

• Inspiratory pressure: ventilator maintains this pressure for the given inspiratory time and the volume achieved by this varies depending on the patient’s respiratory mechanics
• PEEP: positive end-expiratory pressure, the pressure above the atmosphere in the patient’s lungs at the end of expiration
• Respiratory rate
• I:E ratio or inspiratory time (one or the other)
• Fio2

Studies have found no statistically significant differences in mortality, oxygenation or work of breathing between pressure or volume-controlled ventilation.

Describe the graphics used in the mode.

Pressure control

• Rectangular pressure time trace: baseline pressure is PEEP, increases with inspiration to the peak inspiratory airway pressure, maintained at the peak inspiratory pressure during inspiration then decreases back to PEEP with expiration
• Decelerating ramp flow pattern for the flow time waveform  flow reaches zero if inspiratory time and expiratory time is long enough
• Volume time waveform is triangular shaped, variable volume depending on compliance

 

What are the advantages and disadvantages of this mode?

Advantages:

• Increased mean airway pressure (theoretically, mean airway pressure is maintained for a longer amount of time so may increase oxygenation)
• Protective against barotrauma (pressure limits set and reduced peak pressure)
• Increased duration of alveolar recruitment
• More homogenous ventilation
• May improve work of breathing for patients: Offers the highest level of flow at the start of breath when patient flow demand is often greatest  may improve patient-ventilator synchrony

Disadvantages:

• Variable tidal volume as depends on respiratory compliance  if not monitored, then can have volutrauma as compliance improves
• Does not guarantee a certain minute ventilation