Moderately prolonged permissive hypotension results in reversible metabolic perturbation evaluated by intracerebral microdialysis - an experimental animal study

Abstract Background Damage control resuscitation (DCR) and damage control surgery (DCS) is the main strategy in patients with uncontrollable hemorrhagic shock. One aspect of DCR is permissive hypotension. However, the duration of hypotension that can be tolerated without affecting the brain is unknown. In the present study we investigate the effect of 60 min severe hypotension on the brain’s energy metabolism and seek to verify earlier findings that venous cerebral blood can be used as a marker of global cerebral energy state. Material and methods Ten pigs were anaesthetized, and vital parameters recorded. Microdialysis catheters were placed in the left parietal lobe, femoral artery, and superior sagittal sinus for analysis of lactate, pyruvate, glucose, glycerol, and glutamate. Hemorrhagic shock was induced by bleeding the animal until mean arterial pressure (MAP) of 40 mmHg was achieved. After 60 min the pigs were resuscitated with autologous blood and observed for 3 h. Results At baseline the lactate to pyruvate ratios (LP ratio) in the hemisphere, artery, and sagittal sinus were (median (interquartile range)) 13 (8–16), 21 (18–24), and 9 (6–22), respectively. After induction of hemorrhagic shock, the LP ratio from the left hemisphere in 9 pigs increased to levels indicating a reversible perturbation of cerebral energy metabolism 19 (12–30). The same pattern was seen in LP measurements from the femoral artery 28 (20–35) and sagittal sinus 22 (19–26). At the end of the experiment hemisphere, artery and sinus LP ratios were 16 (10–23), 17 (15–25), and 17 (10–27), respectively. Although hemisphere and sinus LP ratios decreased, they did not reach baseline levels (p < 0.05). In one pig hemisphere LP ratio increased to a level indicating irreversible metabolic perturbation (LP ratio > 200). Conclusion During 60 min of severe hypotension intracerebral microdialysis shows signs of perturbations of cerebral energy metabolism, and these changes trend towards baseline values after resuscitation. Sagittal sinus microdialysis values followed hemisphere values but were not distinguishable from systemic arterial values. Venous (jugular bulb) microdialysis might have a place in monitoring conditions where global cerebral ischemia is a risk.

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Anesthetic management of a patient with hollow viscus perforation due to blunt abdominal trauma with grade IV hemorrhagic shock

Anaesthesia, Pain & Intensive Care ◽

10.35975/apic.v25i2.1474 ◽

2021 ◽

Vol 25 (2) ◽

Author(s):

Reza Widianto Sudjud ◽

Djoni Kusumah Pohan ◽

Muhammad Budi Kurniawan ◽

Hana Nur Ramila

Keyword(s):

Hemorrhagic Shock ◽

Blunt Abdominal Trauma ◽

Massive Transfusion ◽

Damage Control ◽

Anesthetic Management ◽

Hollow Viscus ◽

Permissive Hypotension ◽

Massive Transfusion Protocol ◽

Transfusion Protocol ◽

Hollow Viscus Perforation

Hemorrhagic shock is a form of hypovolemic shock in which severe blood loss leads to inadequate oxygen delivery at the cellular level. Death from hemorrhage represents a substantial global problem, with more than 60,000 deaths per year in the United States and an estimated 1.9 million deaths per year worldwide, 1.5 million of which result from physical trauma. This case report aims to stress the need of handling cases of hemorrhagic shock in accordance with damage control protocol. Hemorrhagic shock management using permissive hypotension management, bleeding control, massive transfusion protocol (MTP), minimal crystalloid therapy, and adjuvant therapy is the best approach to get optimal outcome to prevent triad of death. In this case, the application of damage control resuscitation has not been fully implemented because of several constraints. Key words: Hemorrhage; Hemorrhagic shock; Permissive hypotension; Massive Transfusion Protocol; MTP; Resuscitation; Damage control Citation: Pohan DK, Sudjud RW, Kurniawan MB, Ramila HN. Anesthetic management on patient with hollow viscus perforation due to blunt abdominal trauma with grade IV hemorrhagic shock. Anaesth. pain intensive care 2021;25(2):217-221. DOI: 10.35975/apic.v25i2.1474 Received: 11 January 2021, Reviewed: 15 January 2021, Accepted: 16 February 2021

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Cerebral energy metabolism following fluid-percussion brain injury in cats

Journal of Neurosurgery ◽

10.3171/jns.1988.68.4.0594 ◽

1988 ◽

Vol 68 (4) ◽

pp. 594-600 ◽

Cited By ~ 73

Author(s):

Andreas W. Unterberg ◽

Bruce J. Andersen ◽

Geoff D. Clarke ◽

Anthony Marmarou

Keyword(s):

Brain Injury ◽

Energy Metabolism ◽

Glucose Consumption ◽

Tissue Ph ◽

Content Type ◽

Cerebral Energy Metabolism ◽

Fluid Percussion ◽

Metabolic Perturbation ◽

Fine Print ◽

Observation Period

✓ Clinical and experimental evidence suggests that head injury can cause alterations of cerebral energy metabolism. However, the etiology of this metabolic perturbation is not known. The objective of this study was to determine the effect of fluid-percussion trauma on cerebral energy metabolism. Seven ventilated, chloralose-anesthetized cats were subjected to a 3.2-atm fluid-percussion brain injury. Before and for 8 hours after trauma, continuous phosphorus-31 magnetic resonance spectrography was obtained to noninvasively monitor tissue pH, phosphocreatine (PCr), and inorganic phosphate (Pi) levels. Measurement of cerebral blood flow (CBF) by the radioactive microsphere technique and calculation of oxygen and glucose consumption (CMRO2 and CMRGl) were also performed before trauma as well as 30 minutes and 1,2,4, and 8 hours after trauma. The data showed a moderate decrease in tissue pH from 7.04 to 6.89 at 30 minutes following trauma with return to control levels by 3 hours posttrauma. During the 8-hour observation period, CBF, CMRO2, and CMRGl remained at control levels. Tissue PCr and Pi levels were also unchanged. Fluid-percussion trauma at the 3.2-atm level in ventilated cats causes a moderate and transient decrease in tissue pH that returns to control levels after trauma. No other metabolic changes are seen later than 30 minutes posttrauma. This indicates that a mild metabolic disturbance occurs after trauma in the ventilated animal and quickly returns to normal.

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CEREBRAL ENERGY METABOLISM AFTER COMBINED TRAUMATIC BRAIN INJURY AND HEMORRHAGIC SHOCK

Shock ◽

10.1097/00024382-200209001-00057 ◽

2002 ◽

Vol 18 (Supplement) ◽

pp. 21-22

Author(s):

H. Rensing ◽

A. Mautes ◽

D. Thome ◽

M. Bauer

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Energy Metabolism ◽

Hemorrhagic Shock ◽

Cerebral Energy Metabolism

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Assessment of critical thresholds for cerebral perfusion pressure by performing bedside monitoring of cerebral energy metabolism

Neurosurgical FOCUS ◽

10.3171/foc.2003.15.6.5 ◽

2003 ◽

Vol 15 (6) ◽

pp. 1-8 ◽

Cited By ~ 39

Author(s):

Carl-Henrik Nordström

Keyword(s):

Energy Metabolism ◽

Cerebral Perfusion Pressure ◽

Cerebral Perfusion ◽

Perfusion Pressure ◽

Critical Threshold ◽

Intracerebral Microdialysis ◽

Cerebral Energy Metabolism ◽

Neurological Intensive Care ◽

Biochemical Analyses ◽

The Individual

An intractable increase in intracranial pressure (ICP) leading to a progressive decrease in cerebral perfusion pressure (CPP) and cerebral blood flow (CBF) is the dominating cause of death in patients with severe brain trauma. Arterial hypotension may further compromise CPP (and CBF) and significantly contributes to death. In addition, the injured brain is sensitive to raised CPP due to an increased permeability of the blood–brain barrier (BBB) to crystalloids and an impaired pressure autoregulation of the CBF. Given these circumstances, an increase in CPP will cause a net transport of water across the BBB and a further elevation in ICP. Accordingly, the assessment of the lower critical threshold for CPP is important for neurological intensive care. This level varies among different patients and different areas of the brain. In fact, the penumbral zones surrounding focal brain lesions appear to be the most sensitive. In the individual patient, preservation of normal cerebral energy metabolism within areas at risk during a decrease in CPP can be guaranteed by performing intracerebral microdialysis and bedside biochemical analyses.

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