Case Overview

A 36-year-old, 65 kg male patient presented with multiple traumatic injuries. He had sustained a flail chest involving ribs 4–8, which was surgically fixed a week earlier. Additional injuries included pulmonary contusion, L-spine fracture, multiple long bone fractures, and a Grade IV splenic laceration.

At baseline, his heart rate was 98 beats per minute, blood pressure was 170/110 mmHg, and oxygen saturation was 98% on 10 L/min of oxygen. During intraoperative monitoring, urine output was 100 mL in the first hour but fell to 60 mL in the second hour with concentrated urine. Following a 500 mL crystalloid bolus, urine output improved to 100 mL/hr.

Induction and Pharmacology

The choice of induction agents was guided by the need to secure the airway, provide analgesia, and minimize hemodynamic instability in a polytrauma patient with elevated blood pressure and reduced circulating blood volume.

• Glycopyrrolate (0.2 mg): This quaternary ammonium antimuscarinic blocked M2 and M3 receptors, reducing acetylcholine-mediated vagal tone and secretions. It prevented bradycardia and lowered aspiration risk in a trauma patient with airway concerns while also reducing airway resistance.
• Midazolam (1 mg): By enhancing GABA-A receptor activity, midazolam reduced neuronal excitability, stress hormone release, and sympathetic overactivity. This provided anxiolysis, amnesia, and a degree of blood pressure stabilization.
• Fentanyl (200 mcg, pre-induction): As a mu-opioid agonist, fentanyl blunted the stress response to intubation and reduced vascular resistance and myocardial oxygen demand, which was important in the setting of severe hypertension.
• Dexamethasone (8 mg): Acting as a glucocorticoid, it stabilized cell membranes, suppressed inflammatory cytokines, and improved alveolar function by reducing pulmonary edema from the contusion.
• Propofol (50 mg): This GABA-A agonist induced hypnosis but also caused vasodilation and reduced venous return, lowering blood pressure from 170/110 to 130/80 mmHg. Its effects were potentiated by hypovolemia and fentanyl co-administration.
• Atracurium (40 mg bolus followed by 19.5–39 mg/hr infusion): Provided muscle relaxation for intubation and fracture stabilization. Its organ-independent metabolism made it suitable in the presence of liver dysfunction.
• Dexmedetomidine (0.2–0.7 mcg/kg/hr, ~13–45 mcg/hr): As an α2-adrenergic agonist, it reduced norepinephrine release, providing sedation and analgesia with minimal respiratory depression—ideal for pulmonary contusion.
• Paracetamol (1 g IV): Offered analgesia by inhibiting central COX-2 activity, thereby reducing opioid requirements.
• Magnesium sulfate (2 g bolus): Acted as an NMDA receptor antagonist, providing additional analgesia and neuromuscular stabilization.

Hemodynamic Response

Following induction, the patient’s heart rate rose from 98 to 110 bpm, likely compensating for reduced vascular resistance and low intravascular volume. Blood pressure dropped significantly from 170/110 to 130/80 mmHg due to the vasodilatory effects of propofol and fentanyl, compounded by relative hypovolemia.

Management strategies included titrating induction drugs in lower doses, considering etomidate for hemodynamic stability, using an arterial line for invasive blood pressure monitoring, and administering crystalloid boluses (2–2.5 L in total).

Ventilation Strategy

The patient’s ventilatory management had to address flail chest, pulmonary contusion, and the risk of ventilator-induced lung injury (VILI).

Lung injury involved surfactant loss, alveolar collapse, and inflammation. Initial volume-controlled ventilation produced high plateau pressures of 35 cmH₂O and peak pressures of 39 cmH₂O. This risked overstretching alveoli and worsening VILI.

Switching to pressure-controlled ventilation improved compliance. Inspiratory pressure was set at 23–25 cmH₂O, delivering tidal volumes of ~425 mL (6.5 mL/kg), with a PEEP of 6 cmH₂O and respiratory rate 14–18. End-tidal CO₂ was maintained at 30–35 mmHg. The strategy prioritized limiting plateau pressures to <30 cmH₂O and driving pressure to <15 cmH₂O, in line with ARDSnet principles.

End-of-Surgery ABG

At the end of surgery, arterial blood gases showed pH 7.28, PaCO₂ 58 mmHg, PaO₂ 93 mmHg, HCO₃⁻ 26 mEq/L, and lactate 0.9 mmol/L. This represented hypercapnic respiratory acidosis with renal compensation. The normal lactate indicated adequate tissue perfusion despite trauma and surgery.

Elective ventilation was continued to prevent fatigue, worsening hypercapnia, and secondary neurological complications, particularly given the spine fracture.

Fluids and Hemodynamics

Intraoperative fluid therapy consisted of 2–2.5 L crystalloids, 1 L Gelofusine, 2 units PRBC, and 3–4 units FFP. PPV was used to guide resuscitation. A bolus of 500 mL crystalloid improved urine output from 60 mL/hr to 100 mL/hr, indicating restoration of renal perfusion. Targets included maintaining urine output above 0.5 mL/kg/hr and MAP between 65–70 mmHg.

Transfusion aimed to maintain hemoglobin between 7–9 g/dL and INR below 1.5. Norepinephrine was reserved for hypotension unresponsive to fluids.

Coagulation and Liver Function

The patient’s INR was elevated at 1.8, with AST 112 U/L, ALT 68 U/L, albumin 2.9 g/dL, and total bilirubin 1.5 mg/dL. This suggested liver dysfunction secondary to trauma and hypoperfusion.

Management included correcting coagulopathy with plasma, vitamin K, and monitoring for micro-clotting. Atracurium was used as the neuromuscular blocker of choice due to its non-hepatic metabolism.

Analgesia

Given the risk of respiratory suppression, a multimodal analgesic plan was adopted. This included intravenous paracetamol, magnesium, dexmedetomidine, and limited doses of fentanyl.

Regional analgesia was provided with an ultrasound-guided femoral nerve block using ropivacaine (20–30 mL, 0.2%) combined with dexmedetomidine (25 mcg) and dexamethasone (8 mg) as adjuvants. Spinal techniques were avoided due to coagulopathy and L-spine fracture.

Postoperative Care

The patient was electively ventilated in the ICU using PCV with 6–8 mL/kg tidal volumes, PEEP of 5–10 cmH₂O, and a target PaCO₂ of 35–45 mmHg. Daily monitoring included ABG, chest imaging, liver function, INR, urine output, and neurological status.

Weaning to pressure support ventilation was planned once PaCO₂ normalized and plateau pressure was consistently <30 cmH₂O.

Summary

This polytrauma patient with flail chest, pulmonary contusion, liver dysfunction, and coagulopathy required carefully titrated induction, lung-protective ventilation, goal-directed fluid therapy, and multimodal analgesia. Key challenges included managing hypercapnia, avoiding ventilator-induced lung injury, correcting coagulopathy, and maintaining end-organ perfusion. Elective postoperative ventilation, combined with close monitoring of acid-base status, coagulation, and renal function, was critical for optimizing recovery.