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Pleural Tapping (Thoracentesis)

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Indications

• New pleural effusion of unknown cause
• Evaluation for infection, malignancy, or systemic disease

• Symptomatic large pleural effusion causing dyspnea or hypoxemia
• Relief of tension hydrothorax

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Contraindications

• Loculated effusion (use real-time ultrasound guidance)
• Coagulopathy / anticoagulation - Note: Evidence does not support routine correction of INR or platelet count before the procedure when ultrasound-guided. A large retrospective study of 1,009 ultrasound-guided thoracenteses found no significant difference in bleeding rates even with mean INR of 1.9 and platelets <50 x10⁹/L
• Patients on clopidogrel (some increased bleeding risk reported)
• Mechanical ventilation (higher pneumothorax risk)
• Small effusion (<10 mm on lateral decubitus film) - requires ultrasound guidance
• Skin infection overlying the intended insertion site
• Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 1724

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Equipment

• Pfenninger and Fowler's Procedures for Primary Care, p. 682

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Patient Positioning

• Preferred position: Patient seated upright, leaning slightly forward with arms resting on a padded table. This keeps free-flowing fluid in the posterior dependent location.
• Debilitated/supine patients: Lateral decubitus position, lying on the side of the effusion, back near the bed edge. Access is via the mid-scapular or posterior axillary line.
• Important: Do not change patient position between the final ultrasound scan and needle insertion, as fluid can shift.
• Pfenninger and Fowler's Procedures for Primary Care, p. 682

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Ultrasound Guidance

• Identifies a safe insertion site, depth, and angle of entry
• Reduces pneumothorax risk (supported by meta-analysis)
• Identifies aberrant intercostal vessels using a vascular probe
• Simple pleural fluid appears anechoic (black) between the parietal and visceral pleura

• The "curtain sign" - intermittent respirophasic movement of lung into the needle path - means insertion is unsafe at that point; choose a different site
• Echogenic material or septations suggest a complex exudate or loculated effusion
• Pleural thickening >3 mm suggests an exudative effusion
• After the procedure, scan the anterior chest for lung sliding to exclude pneumothorax
• Fishman's Pulmonary Diseases and Disorders; Murray & Nadel's Textbook of Respiratory Medicine, p. 586

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Step-by-Step Procedure

Step 1 - Site Selection

1. Identify the effusion by percussion (dullness), auscultation (reduced breath sounds), and chest radiograph (PA, lateral, lateral decubitus views)
2. Select the insertion site one to two interspaces below the upper fluid level, 5-10 cm lateral to the spine
3. Never insert below the 8th intercostal space posteriorly (risk of liver, spleen, or diaphragm laceration)
4. Never puncture medial to the mid-clavicular line (risk of internal mammary vessel injury)
5. Mark the site with a marker or firm pressure from a needle hub
6. Perform a time-out to verify patient identity and correct side

Step 2 - Skin Preparation and Draping

1. Apply povidone-iodine or chlorhexidine to a wide area
2. Drape with a fenestrated sterile drape or sterile towels
3. Maintain full sterile technique throughout

Step 3 - Local Anaesthesia

1. Raise a skin wheal with 1-2% lidocaine using a 25-gauge needle
2. Switch to a 22-gauge 1.5" needle; angle it slightly downward toward the superior border of the rib
3. "Walk" the needle over the top of the rib (avoids the neurovascular bundle which runs in the costal groove under the rib below)
4. Aspirate and inject as you advance through the intercostal muscle layers
5. Continue advancing until a "pop" is felt (or fluid/air is aspirated), confirming pleural space entry
6. Note the depth; optionally clamp the needle at skin level to mark depth
7. Withdraw the anesthesia needle

If no fluid is obtained at this stage, ultrasound guidance is mandatory before proceeding.

Step 4 - Needle/Catheter Insertion

1. With the larger aspiration needle (18-gauge for air, 15-gauge for fluid) or catheter-over-needle assembly attached to a 50-mL syringe and 3-way stopcock:
2. Pierce skin at the marked site
3. Advance the needle over the superior rib surface (same principle as anesthesia)
4. Aspirate continuously while advancing; stop advancing once pleural fluid is obtained
5. If using catheter-over-needle: slide the catheter off the needle into the pleural space, then withdraw the needle
6. Stabilize the shaft with the non-dominant hand during advancement to prevent over-penetration

Step 5 - Fluid Aspiration

• Collect ~60 mL into a syringe for analysis
• Distribute to specimen tubes immediately

• Connect tubing to vacuum bottles
• Use the 3-way stopcock to direct flow between the pleural space and the drainage container
• Maximum volume: <1.5 L per session (to minimize risk of re-expansion pulmonary oedema)
• Stop immediately if the patient develops cough, dyspnea, or chest pain (may indicate lung re-expansion or non-expandable lung)

Step 6 - Removal and Dressing

1. Ask the patient to perform a Valsalva manoeuvre or hum (raises intrathoracic pressure to minimize air entry)
2. Remove the needle/catheter at end-expiration
3. Apply an occlusive dressing over the site
4. Keep dressing on for 24 hours

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Post-Procedure Management

• Check pulse oximetry after the procedure; hypoxaemia is common due to V/Q mismatch in the re-expanded lung. Provide supplemental oxygen as needed.
• Post-procedure chest radiograph is NOT routinely required. It IS indicated if:
  • Air was aspirated during the procedure
  • Patient is on mechanical ventilation
  • Patient develops cough, chest pain, hypoxia, or dyspnoea
  • Multiple needle passes were made
• Instruct patient to report increased shortness of breath, fever, or redness at the puncture site
• Pfenninger and Fowler's Procedures for Primary Care, p. 682-684

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Pleural Fluid Analysis

• Blood-stained: trauma, malignancy, pulmonary infarction, pneumonia
• White/milky: lipid-rich (chylothorax or pseudochylothorax)
• Purulent, malodorous: empyema
• Food particles: oesophageal rupture

• Pleural fluid protein/serum protein >0.5
• Pleural fluid LDH/serum LDH >0.6
• Pleural fluid LDH >2/3 upper limit of normal serum LDH
• Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 257

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Complications

• Pfenninger and Fowler's Procedures for Primary Care, p. 684

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Key Safety Rules (Summary)

1. Always insert just above the rib - never below it (neurovascular bundle runs in the costal groove inferiorly)
2. Always use ultrasound guidance for small, loculated, or high-risk effusions
3. Never insert below the 8th intercostal space posteriorly
4. Never puncture medial to the mid-clavicular line
5. Never withdraw a catheter back over the needle (catheter shear)
6. Limit therapeutic drainage to <1.5 L per session
7. Do a time-out before the procedure

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Hemorrhagic Stroke with Severe Abdominal Distension

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Why Abdominal Distension Occurs in Hemorrhagic Stroke

1. Neurogenic (Paralytic) Ileus - Most Common

• Stroke-related autonomic dysfunction disrupts normal gut motility
• The enteric nervous system relies on intact CNS-autonomic signaling; mass lesions (especially brainstem, thalamic, or large hemispheric hemorrhages) suppress normal peristaltic drive
• Immobility, sedation, and opioid analgesia all compound the problem
• Presents with progressive abdominal distension, absent bowel sounds, intolerance of enteral feeding

2. Acute Gastric Dilatation

• Rapid gastric distension from swallowed air, loss of gag reflex, or mask ventilation prior to intubation
• Can cause respiratory compromise and aspiration

3. Cushing's (Stress) Ulcer with GI Hemorrhage

• Brain injury - especially raised ICP - drives vagal hyperactivity and gastric acid hypersecretion
• ICH patients are at significant risk of upper GI bleeding
• Can present with abdominal distension from an ileus triggered by GI blood irritating the bowel

4. Intra-abdominal Hemorrhage (in anticoagulated patients)

• ICH may coexist with systemic anticoagulation (e.g., warfarin, NOACs)
• Retroperitoneal or intraperitoneal bleeding following anticoagulation reversal or traumatic fall can cause massive distension
• Must be actively excluded if the patient was anticoagulated or had a fall

5. Abdominal Compartment Syndrome (ACS)

• Rare but life-threatening; can develop from massive fluid resuscitation in a critically ill stroke patient
• IAP >20 mmHg with new organ dysfunction defines ACS
• Critically important because raised IAP directly raises ICP (via raised intrathoracic pressure - impaired venous drainage - raised CVP - impaired cerebral venous outflow)

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The ICP-IAP Interaction: A Critical Danger

Raised IAP
    → Elevates diaphragm
    → Raises intrathoracic pressure
    → Impairs superior vena caval return and jugular venous drainage
    → Raises central venous pressure (CVP)
    → Impairs cerebral venous outflow
    → RAISES INTRACRANIAL PRESSURE (ICP)
    → Reduces cerebral perfusion pressure (CPP = MAP - ICP)
    → Worsens secondary brain injury

• Plum and Posner's Diagnosis and Treatment of Stupor and Coma; Current Surgical Therapy 14e

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Initial Assessment

Immediate priorities

ICH Scoring (Primary ICH Score)

• Score 0-1: ~0% 30-day mortality; Score 4-6: ~97% 30-day mortality
• Plum and Posner's Diagnosis and Treatment of Stupor and Coma, p. 570

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Management of Hemorrhagic Stroke (ICH)

1. Blood Pressure Control

• Target systolic BP ≤140 mmHg (IV nicardipine 5-15 mg/hr infusion, or labetalol 20-80 mg IV bolus)
• If SBP >220 mmHg, more aggressive reduction is warranted
• Avoid excessive reduction - impaired autoregulation in ICH makes the brain pressure-passive; CPP target of 50-70 mmHg
• Risk factors for hematoma expansion: uncontrolled hypertension, hyperglycemia, antithrombotic use, large initial volume, liver disease

2. Coagulopathy Reversal (Urgent)

• Anticoagulant-associated ICH requires emergent reversal:
  • Warfarin: IV Vitamin K + 4-factor PCC (prothrombin complex concentrate) - faster than FFP
  • Dabigatran: Idarucizumab
  • Factor Xa inhibitors (rivaroxaban, apixaban): Andexanet alfa or 4-factor PCC
  • Heparin: Protamine sulfate
• Antiplatelet drugs: Platelet transfusion may be considered but evidence is limited

3. ICP Management

• Elevate head of bed 30-45° (CRITICAL NOTE: abdominal distension may be worsened by this; maintain if ICP is the priority)
• Avoid hypotonic fluids (worsen cerebral oedema)
• Osmotherapy: IV mannitol 0.25-1.0 g/kg, or 23.4% hypertonic saline
• External ventricular drain (EVD) if intraventricular hemorrhage or hydrocephalus
• Target ICP <20-22 mmHg; CPP 50-70 mmHg
• Avoid Valsalva manoeuvres, coughing, straining - all raise ICP

4. Surgical Intervention

• Cerebellar hemorrhage >3 cm causing brainstem compression or hydrocephalus: emergent surgical evacuation
• Supratentorial ICH: surgical benefit remains limited; consider for young patients with accessible lobar hemorrhage and neurological deterioration
• External ventricular drainage for symptomatic obstructive hydrocephalus

5. Seizure Management

• Non-convulsive status epilepticus occurs frequently in ICH; continuous EEG monitoring is recommended for patients with unexplained impaired consciousness
• Prophylactic anticonvulsants are NOT routinely recommended
• Treat confirmed seizures with levetiracetam or valproate

6. General Critical Care

• Strict normoglycaemia (hyperglycaemia worsens ICH outcomes)
• Normothermia (fever raises cerebral metabolic demand)
• DVT prophylaxis: intermittent pneumatic compression devices (NOT pharmacological initially, given active bleeding)
• ICU admission with arterial line and central venous access
• Plum and Posner's Diagnosis and Treatment of Stupor and Coma, p. 571

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Management of Severe Abdominal Distension

Step 1 - Nasogastric (NG) Tube Decompression (FIRST PRIORITY)

• Insert NG tube immediately for:
  • Gastric decompression (reduces IAP and aspiration risk)
  • Administration of enteral medications (including antiepileptics, antihypertensives)
  • Enteral feeding when ileus resolves

Step 2 - Identify the Cause

• CT abdomen/pelvis to exclude:
  • Mechanical small/large bowel obstruction (requires surgical referral)
  • Intra-abdominal/retroperitoneal hemorrhage
  • Mesenteric ischemia (rare but catastrophic)
• Plain abdominal X-ray: air-fluid levels, massively dilated colon (Ogilvie's syndrome)

Step 3 - Treat Paralytic Ileus / Neurogenic Gut Dysmotility

• Correct electrolytes: hypokalaemia, hypomagnesaemia, and hypophosphataemia all inhibit gut motility - correct urgently
• Reduce or eliminate opioids where neurologically safe
• Avoid excessive IV fluid hydration (bowel oedema worsens ileus)
• Early mobilisation as neurological status allows
• Consider neostigmine 2 mg IV (under cardiac monitoring) for acute colonic pseudo-obstruction (Ogilvie's syndrome) if caecal diameter >12 cm and no response to conservative measures

Step 4 - Intra-abdominal Pressure Monitoring

• Measure IAP via Foley catheter (instil 25 mL saline, measure pressure at end-expiration)
• IAP grading:
  • Grade I: 12-15 mmHg
  • Grade II: 16-20 mmHg
  • Grade III: 21-25 mmHg
  • Grade IV: >25 mmHg = Abdominal Compartment Syndrome
• If ACS develops: decompressive laparotomy is the definitive treatment (and directly reduces ICP in the process)

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Combined Management: Competing Priorities

Key Decision Framework:

1. Secure airway first - both conditions (reduced GCS from ICH + distension from ileus) independently mandate early intubation
2. NG decompression is non-negotiable - reduces IAP, reduces aspiration risk, enables medication delivery
3. Reverse coagulopathy urgently for ICH - this is the single most impactful acute intervention
4. Monitor IAP continuously - IAP >20 mmHg in a patient with impaired cerebral autoregulation is a neuro-emergency
5. Do not allow IAP to rise unchecked - the ICP consequences are direct and severe
6. Neurosurgical + General Surgery involvement simultaneously if ACS develops alongside ICH

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Summary: Priority Action List

• Plum and Posner's Diagnosis and Treatment of Stupor and Coma, p. 571-572; StatPearls - Hemorrhagic Stroke Overview

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Further Management of Abdominal Distension (in Hemorrhagic Stroke)

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Step 1: Continuous Monitoring and Serial Assessment

Intra-abdominal Pressure (IAP) Measurement

• Measure IAP every 4-6 hours in at-risk patients
• Abdominal Perfusion Pressure (APP) = MAP - IAP; target APP >60 mmHg
• Monitor for organ dysfunction signatures: ↑peak airway pressure, ↓urine output, ↑lactate, ↑creatinine, ↑ICP
• Current Surgical Therapy 14e, p. 1418-1419

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Step 2: Non-Surgical Decompression Measures (First-Line)

A. Gastric and Luminal Decompression

• Nasogastric (NG) tube: Insert if not already done. Decompress gastric content and swallowed air. Leave on free drainage. Confirm position on X-ray.
• Rectal tube: For large bowel gas accumulation (especially Ogilvie's syndrome/acute colonic pseudo-obstruction). Insert a large bore flatus/rectal tube and connect to a bag. Can achieve dramatic reduction in colonic distension.
• Both maneuvers have direct evidence of reducing IAP.

B. Correct Electrolyte and Metabolic Derangements

C. Prokinetic Agents

Caution with neostigmine in ICH: Bradycardia is a common side effect. Have atropine (0.6 mg IV) available at the bedside. Avoid if the patient has active bronchospasm, mechanical obstruction, or severe bradycardia at baseline. The benefit of lowering IAP (and thus ICP) generally outweighs the risk if colonic pseudo-obstruction is the cause.

• Goodman & Gilman's Pharmacological Basis of Therapeutics

D. Optimise Fluid Management

• Avoid excessive IV crystalloid - each litre of crystalloid worsens visceral and bowel wall oedema, which directly raises IAP
• Use balanced crystalloids (Hartmann's/Ringer's Lactate) over normal saline (less bowel oedema)
• Consider colloid or albumin replacement if hypovolaemic (less oedema-promoting)
• Reassess fluid balance 4-hourly; target euvolaemia, not liberal positive balance
• If the patient has ascites: consider ultrafiltration (in renal failure context) or therapeutic paracentesis to directly reduce IAP

E. Body Positioning

• Elevate head of bed 30-45° (already mandated for ICP management in ICH) - this is compatible with abdominal management
• Avoid Trendelenburg position - worsens IAP and ICP simultaneously
• Lateral decubitus or prone positioning may improve abdominal drainage in selected cases but is rarely feasible in active ICH

F. Remove or Reduce Aggravating Medications

• Opioids: Reduce or substitute with non-opioid analgesia (paracetamol, low-dose ketamine, regional nerve blocks where feasible) - opioids are the most potent inhibitors of gut motility in ICU
• Anticholinergics: Avoid atropine, hyoscine, tricyclics
• Vasopressors: High-dose noradrenaline reduces mesenteric blood flow and worsens ileus - optimise to minimum effective dose

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Step 3: Specific Cause-Directed Interventions

A. Acute Colonic Pseudo-Obstruction (Ogilvie's Syndrome)

1. All Step 2 measures above
2. Neostigmine 2 mg IV (first-line pharmacological - 80-90% response rate)
3. If no response after 24h: colonoscopic decompression (place decompression tube in right colon; do not insufflate)
4. If perforation or ischaemia: surgical caecostomy or right hemicolectomy

• 12 cm: pharmacological treatment mandatory

• 14 cm or rapidly expanding: colonoscopic decompression should not be delayed

• Perforation risk rises sharply above these thresholds

B. Large-Volume Ascites Contributing to Distension

• Percutaneous image-guided paracentesis (bedside, ultrasound-guided) can drain large volumes directly - reduces IAP and ICP in the same procedure
• Drain >1 L to have significant IAP impact (Comprehensive Clinical Nephrology)
• Replace with IV albumin (6-8 g per litre drained beyond 5 L) to prevent post-paracentesis circulatory dysfunction
• Coordinate with assessment of any coagulopathy before drainage in ICH context

C. Intra-abdominal Hemorrhage / Haematoma

• If CT confirms retroperitoneal or intraperitoneal bleed:
  • Ensure coagulopathy is reversed (already underway for ICH)
  • If actively bleeding: CT angiography to identify bleeding vessel; IR-guided embolisation as first-line (avoids general anaesthesia risk)
  • If haematoma is causing ACS without active bleeding: percutaneous drain after coagulopathy corrected
  • Surgery is last resort given concurrent active ICH

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Step 4: Escalation to Surgical Decompression (ACS)

Decompressive Laparotomy

• Definitive treatment for ACS
• Generous midline incision through skin AND fascia
• Limited incision is inadequate (analogous to fasciotomy for limb compartment syndrome)
• Abdomen left open (damage control approach) with temporary closure

Intraoperative Confirmation of ACS Diagnosis:

• Immediate improvement in haemodynamics on fascial opening
• Drop in peak airway pressures on ventilator
• Fall in ICP (most relevant in this ICH context)
• Improvement in urine output

Bedside Decompression (when OR transport is impossible):

• Hemodynamic instability preventing transport
• Severely elevated ICP preventing safe movement
• Respiratory failure requiring very high ventilator settings

Temporary Abdominal Closure Options:

• Current Surgical Therapy 14e, p. 1417-1422

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Step 5: Post-Decompression Management

After Laparotomy/Decompression:

• Continue IAP monitoring - recurrent ACS can develop, especially if resuscitation continues or sepsis develops
• Plan for definitive abdominal closure once oedema resolves (usually 48-72h if cause controlled)
• Staged closure with progressive fascial reapproximation at each return to OR
• Nutritional support: start low-rate enteral nutrition as soon as bowel sounds return; avoid prolonged parenteral-only nutrition (worsens gut mucosal atrophy and ileus)
• Abdominal domain restoration: if abdomen cannot be closed primarily, consider component separation or biological mesh

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Special Considerations in Concurrent ICH

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NAVA Mode on Maquet (Getinge) SERVO Ventilators

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Core Principle

P_peak = NAVA level × (Edi_peak − Edi_min) + PEEP

For NIV NAVA: P_peak = NAVA level × (Edi_peak − Edi_min) + PEEP + 2 cmH₂O

• Edi (μV) = electrical signal of diaphragm crura, detected by the Edi catheter
• NAVA level (cmH₂O/μV) = the "gain" factor - how much pressure per μV of Edi signal
• The bigger the patient's neural effort → the larger the Edi → the larger the pressure delivered
• This creates breath-by-breath proportional synchrony between neural drive and ventilator output
• Murray & Nadel's Textbook of Respiratory Medicine; SERVO-U User Manual v4.0

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Required Equipment

The catheter must be removed before any MRI examination.

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Step-by-Step NAVA Workflow on SERVO-i / SERVO-U

Step 1 - Hardware Setup

1. Insert the Edi Module into the designated slot on the SERVO ventilator
2. Connect the Edi Cable to the Edi Module
3. Run the Edi Module function check (automatic self-test on SERVO-U; manual test plug on SERVO-i)
4. Wait for "Edi Module test passed" message. If it fails, replace the cable/module and retest.

Step 2 - Calculate Insertion Depth (NEX Measurement)

• Measure NEX (Nose-Ear-Xiphoid) distance in cm
• Use the SERVO's built-in CALCULATION TOOL (in the Neural Access menu):
  • Enter catheter size, insertion route (oral/nasal), and NEX measurement
  • The ventilator calculates the correct insertion depth (Y cm)
• Alternatively, use the Edi catheter measuring tape

Step 3 - Insert the Edi Catheter

1. Dip the Edi catheter tip in water for a few seconds to activate pre-lubrication
2. Insert nasally or orally to the calculated depth
3. Connect the catheter's cable connector to the Edi Cable

Step 4 - Position the Edi Catheter (CRITICAL STEP)

• Top 2 leads: P waves and QRS complexes clearly visible (near the heart - atria above diaphragm)
• Bottom 2 leads: P waves disappear and QRS amplitude decreases (below the diaphragm)
• 2 middle leads highlighted in PINK/BLUE during inspiration - this means the electrodes are spanning the diaphragm correctly

Once correctly positioned, note and document the insertion length. Secure catheter firmly to prevent displacement.

Step 5 - Evaluate the Edi Signal

• The signal should be 2-20 μV at baseline
• Check for Edi deflections (upward spikes with each breath)
• If the signal is flat/absent: troubleshoot before proceeding (see below)

Step 6 - Set Initial NAVA Level (NAVA Preview)

1. While still in the current conventional mode, open Neural Access → NAVA Preview
2. Two waveforms are displayed simultaneously:
   • Grey curve: estimated pressure based on current Edi × NAVA level
   • Yellow curve: actual current airway pressure in the conventional mode
3. Adjust the NAVA level until the grey (estimated NAVA) curve approximately matches the yellow (current conventional) curve
4. Starting rule: Set the initial NAVA level equal to (or slightly below) the current pressure support level
   • e.g. if currently on PSV 12 cmH₂O, start NAVA level around 1.0-1.5 cmH₂O/μV
5. Press "Close" to transfer the NAVA level to the NAVA mode window

Optional: Perform an expiratory hold and verify that a positive Edi deflection coincides with a negative airway pressure deflection (confirms neural-pneumatic coupling)

Step 7 - Select NAVA Mode and Set All Parameters

All backup settings must be configured before switching to NAVA. The ventilator will not allow NAVA without backup parameters set.

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Understanding the Key Parameters

Edi Signal Values

• Edi_peak <5 μV: Patient over-assisted → decrease NAVA level by 0.1-0.2 cmH₂O/μV
• Edi_peak >20 μV: Patient under-assisted → increase NAVA level by 0.1-0.2 cmH₂O/μV
• Edi_min >5 μV: Lung under-recruited, PEEP too low → increase PEEP by 1 cmH₂O

NAVA Level Titration

• Higher NAVA level → more support per μV → Edi typically falls (negative feedback mechanism)
• Lower NAVA level → less support → Edi rises (patient works harder)
• This self-regulation is a key safety feature of NAVA - the patient's neural drive naturally self-limits over-assistance

Edi Trigger

• Default 0.5 μV
• Must exceed background noise variability (~<0.5 μV baseline noise)
• Too low (<0.5 μV): Over-triggering on noise; auto-triggers; resets apnea timer (patient may appear to be breathing when apnoeic)
• Too high (>1.5-2 μV): Missed triggers; patient effort not detected

Backup Ventilation

• Activates automatically when apnea time elapses without Edi signal
• Switches to Pressure Control at the backup PC level and rate
• Ensures safety if patient becomes apnoeic (CNS depression, oversedation, sleep apnea)
• NIV NAVA: Trigger cannot be manually set - it is automatically set by the ventilator

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NAVA vs Conventional Modes

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Edi-Guided PEEP Titration

• Increase PEEP in small steps; assess Edi min after respiratory drive stabilises
• If Edi min falls: PEEP is appropriate (lung recruits, FRC improves)
• If Edi min rises or stays high at low PEEP: lung atelectasis is driving tonic activity; increase PEEP

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NIV NAVA (Non-Invasive NAVA)

• Same Edi catheter and principles apply
• Pressure delivered: NAVA level × (Edi_peak − Edi_min) + PEEP + 2 cmH₂O (extra 2 cmH₂O to compensate for mask leak)
• Edi trigger is automatically set in NIV NAVA (not manually adjustable)
• Particularly useful for NIV weaning and acute hypercapnic respiratory failure with intact neural drive

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Troubleshooting

Low or No Edi Signal

Increased Edi Signal (Edi_peak >20 μV)

Autotriggering (Phantom Breaths)

• Edi trigger set too low → raise to 1.0-1.5 μV
• Distinguish from true respiratory effort

Frequent Switching to NAVA (PS) Backup

• Patient using accessory muscles triggering pneumatic sensor
• PS flow trigger too sensitive → change to pressure trigger or adjust sensitivity
• Set pneumatic trigger at -8 cmH₂O or below to ensure Edi trigger takes precedence

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Weaning from NAVA

1. Consider weaning when: patient stable, minimal work of breathing, FiO₂ <0.30, PEEP ≤5, Edi peak averaging ~10 μV
2. Decrease NAVA level in 0.2-0.3 cmH₂O/μV increments every 2-4 hours
3. Observe Edi peak for 15-20 min after each change
4. If Edi peak rises significantly: return to previous NAVA level
5. Consider extubation when NAVA level ≤0.5 cmH₂O/μV with acceptable Edi peak and VT
6. After extubation: keep catheter in place for 2 hours to monitor WOB trend via Edi

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Clinical Advantages of NAVA

1. Improved patient-ventilator synchrony - eliminates trigger delays, premature cycling, and delayed cycling caused by pneumatic triggers
2. Proportional unloading - prevents both over-assistance (causing diaphragm atrophy) and under-assistance (causing fatigue)
3. Self-regulation - patient's neural feedback loop naturally prevents runaway pressure delivery
4. Real-time WOB monitoring - Edi is a continuous, objective marker of respiratory drive and effort
5. Edi-guided PEEP titration - uses physiology (not mechanics alone) to set PEEP
6. Applicable across all ages - neonate, paediatric, and adult populations

• SERVO-U User Manual v4.0; Getinge SERVO-i Pocket Guide; StatPearls - NAVA