Serial AKBR Measurements after Hemorrhagic Shock and the Degree of Hepatic Mitochondrial Damage
Toshio Nakatani, MD; Nobuaki Matsuo, MD; Takashi Ishihara, MD; Shigeru Hakota, MD;¹ Akihiko Hirakawa, MD;¹ Hisanori Fukui, MD;¹ Seiichiro Kanzaki, MD;¹ Kenji Nakatani, MD;¹ Kunio Kobayashi, MD²
Department of Emergency and Critical Care Medicine, Kansai Medical University, Osaka, Japan
Trauma and Critical Care Center, Teikyo University School of Medicine, Tokyo, Japan

Introduction: During a profound and prolonged shock, hepatic mitochondria yield to severe, functional, and structural damage that may not recover quickly after fluid resuscitation. It is difficult to assess the mitochondrial damage through conventional hepatic functional tests. Arterial ketone body ratio (AKBR) is a parameter that reflects hepatic mitochondrial redox status, and closely correlates with hepatic energy production, which is a fundamental function of liver mitochondria. Effects of massive hemorrhage on hepatic mitochondrial function with or without cirrhosis were studied by serial measurement of AKBR.

Methods: AKBRs were measured repeatedly in three groups, A, B, and C. Group A consisted of 30 trauma victims admitted due to hemorrhagic shock (systolic blood pressure (BP) <80 mmHg), without any liver disease. Group B were cirrhotic patients admitted due to ruptured esophageal varices, without shock between 1993 and 1998 (n = 24). Group C consisted of cirrhotic patients admitted due to ruptured esophageal varices with shock between 1993 and 1998 (n = 14). The AKBR recovery rate was calculated from the gradient of initial recovery and expressed as Î AKBR/24 hours.

Results: On admission, average systolic BPs were 65 ±3, 122 ±3, and 66 ±3 mmHg; AKBRs were 0.29 ±0.04, 0.49 ±0.04^a, and 0.27 ±0.04; and, AKBR recovery rates were 2.28 ±0.52, 0.21 ±0.04^a, and 0.06 ±0.05^a,b, in groups A, B, and C, respectively (Mean ±SEM^a,b, significant vs. Groups A, B, respectively; p <0.05.). The AKBRs of Groups A and C on admission to the hospital were decreased highly, which reflected reduced hepatic mitochondrial redox status during the shock. After resuscitation, the AKBR levels recovered quickly in Group A, which indicated temporary mitochondrial dysfunction that was due to extrinsic reasons, indicated by markedly decreased AKBR. Although resuscitation was similarly successful, the AKBR recovery rate was low in cirrhotic patients, particularly in those with shock (Group B), which indicated hepatic mitochondria yielded intrinsic damage.

Conclusion: Hepatic mitochondria in cirrhotic patients, are vulnerable to massive hemorrhage, particularly after profound shock. Serial measurement of AKBR enables assessment of the degree of hepatic mitochondrial damage and the extent of the deterioration in hepatic energy metabolism during and shortly after hemorrhagic shock.

Key words: Arterial ketone body ratio (AKBR); assessment; measurements; blood pressure; cirrhosis; hepatic damage; hypovolemia; liver; mitochondrial damage; shock, hemorrhagic; trauma

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