Authors: Dr. Aanchal Bhandari , Dr. Kishalay Datta , Dr. Anita Rawat , Dr. Priya Govil , Dr. Arun Kaushik , Dr. Surjeet Acharya

Abstract

Introduction

Arterial pH levels below 6.8 are traditionally considered incompatible with life due to irreversible cellular dysfunction and poor survival. Severe acidosis with concurrent hyperkalemia and critical anemia presents an exceptional resuscitation challenge. This case describes full recovery in a patient with a pH of 6.75 after traumatic hemorrhagic shock, highlighting how aggressive, multidisciplinary management can reverse physiology once deemed fatal.

Aims / Objectives

To report a trauma patient’s survival and full recovery from extreme acidosis, hyperkalemia, and anemia, underscoring the value of rapid correction and coordinated resuscitation in restoring physiological stability.

Materials / Methods

A multidisciplinary trauma, surgical, and critical care approach was employed using institutional massive transfusion and resuscitation protocols. Serial clinical, hemodynamic, and metabolic assessments guided real-time management, including fluid and blood replacement, electrolyte correction, and definitive surgical intervention.

Case Description

A 42-year-old male with no comorbidities presented 15 minutes after a high-speed motor vehicle collision with GCS 3, pulse 148 bpm, unrecordable BP, RR 32/min, SpO₂ 88% on high-flow oxygen, and capillary refill >5 s. FAST revealed intra-abdominal free fluid. Arterial blood gas showed pH 6.75, HCO₃⁻ 14.1 mmol/L, lactate 7.2 mmol/L, K⁺ 7.1 mmol/L, and Hb 4.8 g/dL. ECG demonstrated sinus tachycardia with peaked T waves and widened QRS complexes. Massive transfusion protocol was activated with 6 units PRBCs, 4 units FFP, and a 5-pack of platelets, alongside crystalloids, tranexamic acid, calcium gluconate, insulin–dextrose, salbutamol, sodium bicarbonate, norepinephrine, and antibiotics. Emergency laparotomy achieved definitive hemorrhage control.

Results

At 45 minutes, repeat ABG showed pH 6.82 with minimal improvement, and surgery proceeded. Intraoperatively, ~3 L hemoperitoneum was evacuated from a grade IV liver laceration and mesenteric tears, followed by damage control packing and temporary closure.

With transfusion and norepinephrine, blood pressure improved from unrecordable to 100/60 mmHg after hemorrhage control and acidosis correction. ECG normalized as acidosis and hyperkalemia resolved; potassium fell rapidly, later requiring mild replacement. Hemoglobin increased to 10.2 g/dL, restoring perfusion.

The patient was extubated on day 4, discharged on day 14, and achieved complete hepatic and neurological recovery at 6 weeks.

Discussion

Survival at a pH of 6.75 is exceptionally rare, as severe acidosis and hyperkalemia typically precipitate fatal arrhythmias. In this case, early recognition, aggressive resuscitation, and simultaneous surgical intervention reversed profound physiological collapse. This case underscores that even extreme acidemia can be survivable with rapid, protocolized, multidisciplinary management.

Conclusion

Profound acidosis with severe hyperkalemia and anemia should not be viewed as futile in trauma resuscitation. Timely, coordinated intervention including massive transfusion, targeted correction of acidosis and electrolytes, and prompt surgical control can achieve complete recovery even in cases with pH <6.8. 

Keywords: Severe acidosis, trauma, resuscitation, hemorrhagic shock