Hemorrhagic Shock

Occurs when blood loss exceeds the body’s ability to compensate, leading to decreased organ perfusion and resultant end organ dysfunction. The body has compensation mechanisms, beginning with peripheral and mesenteric vasoconstriction, which shunts blood to the central circulation. As blood loss continues, the heart rate and respiratory rate increase in an attempt to increase oxygen delivery despite a diminished blood volume. A decrease in tissue perfusion alters the metabolism from aerobic to anaerobic, generating lactate from pyruvate. Thus lactate is a sensitive biomarker when assessing shock and when combined with the Rockall score, has a high positive predictive value of in-hospital death from UGIB.

Shock is initially reversible, but eventually becomes irreversible as cell death –> end organ damage –> multi-system organ failure –> death. ATLS uses four classifications for hemorrhagic shock which is useful in understanding the progressive effect blood loss has on the body, however hemorrhagic shock is SHOCK, and should be dealt with swiftly and aggressively. Moreover, a patient’s age, co-morbidities, and medications (such as a beta-blocker) can alter their presentation, so it is important to treat the patient and not the number. Assessing mental status is a good way to determine end organ perfusion, and mental status changes may be the only presenting sign of shock.

A mnemonic to remember the blood loss stages of hemorrhagic shock uses the scoring system from tennis: Love-15-30-40-Game Over (>40)

Credit: LifeintheFastlane.com

Focus on optimizing oxygenation and perfusion while simultaneously diagnosing and treating the underlying cause of the bleeding!

• 2 large bore IVs or cordis
• Pre-oxygenation for possible RSI*
• Cardiopulmonary monitoring
• Volume repletion (blood products† and crystalloid‡)
• TXA bolus
• Appropriate consultations (such as surgery, OBGYN or MICU)

* Hemorrhagic shock results in diminished perfusion, not decreased oxygen carrying capacity. Oxygen supplementation is often not necessary; and hyperoxia may be detrimental. However, many patients need to be rapidly intubated and pre-oxygenation will buy you more time to pass the tube.

† Actively bleeding patients should be transfused early and continue receiving blood products until bleeding has been controlled, the patient has been stabilized, and the target hemoglobin has been achieved. A restrictive transfusion strategy (Hgb of 7) significantly improves patient outcomes compared to a liberal strategy (Hgb of 9).

Permissive hypotension is controversial, and most studies involve penetrating trauma where the goal is to keep pressures low enough avoid disruption of an unstable clot while maintaining adequate perfusion.

‡ Too high of a crystalloid:blood product ratio can result in a dilutional coagulopathy.

Everyone agrees for the balanced repletion of lost components using RBCs, FFP, and platelets, however the “ideal” ratio is controversial.

Borgman 2007– Retrospective observational study of 246 military patients compared FFP/RBC ratios of 1:8, 1:2.5, and 1:1.4. They found mortality improved with increased FFP:RBC ratio.

Holcomb 2008- Retrospective review of 466 multi-trauma patients compared FFP/RBC <1:2 and ≥ 1:2. They found mortality improved with <1:2 at 6 hours, 24 hours, and 30 days.

Zehtabchi 2009– Retrospective observational review (3 retrospective, 1 prospective cohort) of 1,511 patients. Brings up issues such as high cost of FFP; complications such as volume overload, infections, and nonhemolytic transfusion reactions; and importance of FFP timing (“transfusing 6 units of FFP after completion of transfusion of 6 units of PRBC, while satisfying the 1:1 ratio, does not translate into aggressive treatment of coagulopathy”). They found Inadequate evidence to support or refute high FFP:RBC ratio.

PROPPR 2015- Multi-center RCT of 680 severe trauma patients. Compared FFP:Platelets:RBC ratios of 1:1:1 vs. 1:1:2. They found no difference in mortality at 24 hours or 30 days. However, exsanguination was reduced (14.6% vs 9.2% P=.03) and more hemostasis was achieved (86% vs. 78% P=.006) in the 1:1:1 vs the 1:1:2 group.

The Blakemore has been around since the 1950s and consists of 3 components: a gastric balloon, an esophageal balloon, and a gastric suction port. It is a rescue therapy used to tamponade bleeding, indicated when acute life-threatening bleeding from esophageal or gastric varices do not respond to medical therapy or endoscopic hemostasis or when such treatments are unavailable. There is also a case report of it being used successfully for nonvariceal distal esophageal bleeding after other therapies had failed. It has a high rate of complications, including aspiration pneumonia, esophageal perforation, mucosal necrosis, and respiratory compromise. Always have a low threshold to intubate the patient to reduce risk of aspiration. Never inflate the esophageal balloon prior to inflating the gastric balloon. It is a temporizing measure, as the direct pressure can cause ulcerations.

TXA reduces fibrinolysis by preventing the conversion of plasminogen to plasmin, thereby decreasing the breakdown of blood clots. TXA is used to help achieve hemostasis, and has been shown to have a mortality benefit in acute, life-threatening bleeding from trauma, surgery, and post-partum hemorrhage… so why not use it in UGI bleeds? Well, previous guidelines recommend PPIs and endoscopy as the mainstay of treatment for UGI bleeds. According to the 2014 Cochrane review of 8 RCTs, TXA appears to have a mortality benefit (RR 0.6 P=0.007) compared to placebo. TXA did not significantly decrease re-bleeding when compared to placebo. There was no significant increase in rate of thromboembolic events in the TXA groups. The overall quality of evidence is moderate to low largely due to heterogeneity; and more research is needed. The daily dosage ranged from 4-8g.

The thought is that the majority of bleeding is from a peptic ulcer, so it would seem that neutralizing gastric pH would help increase clot formation to prevent re-bleeding therefore decreasing mortality. A meta-analysis of 6 RCTs totaling 2,223 patients with undifferentiated UGI bleeding compared PPI to either placebo, H2RA, or no treatment prior to endoscopy . PPIs had no significant reduction in death, re-bleeding, or need for surgery compared to the controls. I think David Newman of www.thennt.com summarizes it best: NNT:0 NNH:0, therefore there is no benefit to using PPI prior to EGD.