The Case:

A 21 years old young man was presented to ER at 4 AM with an alleged history of RTA (Road Traffic Accident) , following which he had been in altered sensorium. On evaluation by ER physician and neurosurgeon, he was found to have a large left sided acute SDH (Subdural Hematoma) with midline shift and brainstem distortion. His BP was 130/90 mmhg, Pulse 88/min and Hb 10 gm%. He had also fracture left radius. Other systemic examinations were found to be satisfactory. He underwent emergency craniotomy at 8 AM. At the leg end of the surgery he suffered a cardiac arrest. Patient was revived, ROSC achieved after CPRand shifted to ICU after surgical closure of the craniotomy site. ABG revealed respiratory alkalosis with low haematocrit ( Hb was 3 gm%). Immediate bedside USG revealed hemoperitonium with multiple splenic lacerations. Urgent laparotomy was done and splenectomy performed. Massive blood transfusion was given according to protocol. After shifting back to ICU patient became hemodynamically stableand vasopressins were gradually tapered off. On Post-operative day 1 his sensorium improved satisfactorily. He was shifted from ICU on post-operative day2.  Post-operative day 3 he underwent ORIF (open reduction and internal fixation) with plating for fracture left radius. He recovered well and discharged on post-operative day 10. Later on he underwent elective cranioplasty.

Discussion:

Left upper quadrant pain, Kehr’s sign ( shoulder pain due diaphragmatic irritation by hemoperitonium ) , guarding and rebound tenderness are usually classical presentation of splenic trauma^2,3. But in some situations especially in case of polytrauma or when patient is in altered sensorium these classical findings may be totally absent as in our case. So in trauma cases there should be a high degree of suspicion of injury to other organ system as well. Meticulous hemodynamic monitoring remains the cornerstone in these cases. A low threshold for imaging modalities and multidisciplinary team approach is very much essential in dealing with such disasters.

References:

1. McIndoe, Archibald H. “Delayed haemorrhage following traumatic rupture of the spleen.” British Journal of Surgery78 (1932): 249-268.
2. Farhat GA, Abdu RA, Vanek VW: Delayed splenic rupture: real or imaginary?.Am Surg. 1992, 58: 340-345.
3. Kodikara S: Death due to hemorrhagic shock after delayed rupture of spleen: a rare phenomenon. Am J Forensic Med Pathol. 2009, 30: 382-383. 10.1097/PAF.0b013e3181c03caf.

Author:

1. Dr.Saikat Mallik (Consultant, Laparoscopic & Transplant Surgery Narayana Superspeciality Hospital, Guwahati)
2. Dr. Apurba Kumar Borah (Consultant & HOD, CCEM, Narayana Superspeciality Hospital, Guwahati)

The post Polytrauma: Can be anything appeared first on CCEM Journal.

Over the last 10 years, the management of major hemorrhage in trauma patients has changed radically. This is mainly due to the recognition that many bleeding patients when they come to the emergency have an established coagulopathy before the dilutional effects of fluid resuscitation. Traumatic coagulopathy has been demonstrated in patients who received little or no IV fluid therapy, negating the long-held belief that iatrogenic hemodilution is the main causative factor in traumatic coagulopathy. This has led to the use of new terminology ATC(acute traumatic coagulopathy); trauma induced coagulopathy. The presence of this impairment early after trauma is an important predictor for increased organ dysfunction, infection and overall mortality.

Phases:

Cap and Hunt Classified trauma associated coagulopathies into 3 phases.

• First phase is immediate activation of multiple hemostatic pathways with increased fibrinolysis in association with tissue injury and /or tissue hypo-perfusion.
• Second phase involves therapy related factors during resuscitation.
• Third phase, post resuscitation phase is an acute phase response leading to pro thrombotic state predisposing to venous thromboembolism.

Of these three phases, first phase corresponds to ATC and clinical features of first phase along with the pathophysiologic factors of second phase provide the characteristics of trauma induced coagulopathy.

European management guidelines for trauma induced coagulopathy:

Initial assessment and management:

• Extent of traumatic hemorrhage assessed.
• Patient in shock with identified source of bleeding to be treated immediately.
• Patient in shock with unidentified source of bleeding send for further investigation.
• Coagulation, hematocrit, serum lactate, base deficit assessed.
• Antifibrinolytic therapy (tranexamic acid within 3 hours after injury) initiated.
• Patient with history of anticoagulant therapy assessed.

Resuscitation:

• Systolic blood pressure of 80-90 mm Hg achieved in absence of TBI.
• Measures to achieve normothermia implemented.
• Target Hemoglobin Level 7-9 mg/dl achieved.

Surgical Intervention:

• Damage control surgery performed in hemodynamically unstable patient.

Coagulation management:

• Massive transfusion protocol with high plasma red blood cell ratio employed.
• Target fibrinogen level 1.5 -2g/l achieved.
• Target platelet level achieved.
• Prothrombin complex concentrate administered if indicated due to Vitamin K antagonist,oral anticoagulant or evidence from viscoelastic monitoring.

Conclusion:

Acute traumatic coagulopathy is caused by endogenous factors but can be worsened by improper medical management. Drivers of ATC are activation of protein C, disruption of endothelial glycocalyx, consumption of fibrinogen and exhaustion/ dysfunction of platelets. This result in reduced clot strength, auto-heparinization and hyper fibrinolysis. Patients presenting to emergency with an established coagulopathy are liable to poor outcomes and must be recognized as early as possible and managed directly and aggressively.

Author:

1. Dr. Soumar Dutta, ( Consultant, Critical Care & Emergency Medicine, Narayana Superspeciality Hospital, Guwahati )

2. Dr. Ismat Ara Hussain Choudhury (Fellow, Emergency Medicine Narayana Superspeciality Hospital, Guwahati)

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