Dirigente Medico
Responsabile UAS “Trombosi Venosa Profonda ed Embolia Polmonare”
Responsabile CDF BLSD IRC “Emersan Lateranum”
U.O.C. Medicina Interna I per l’Urgenza

KEY-WORDS: Hypovolemic shock

INTRODUCTION
CLINICAL
WORKUP
TREATMENT
FOLLOW-UP
MISCELLANEOUS
BIBLIOGRAPHY

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INTRODUCTION

Background: Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in multiple organ failure due to inadequate perfusion. For the most part, hypovolemic shock will result secondary to rapid blood loss (hemorrhagic shock).

Acute external blood loss secondary to penetrating trauma or severe gastrointestinal bleeding disorders are two common causes of hemorrhagic shock. Hemorrhagic shock can also result from significant acute internal blood loss into the thoracic and abdominal cavities.

Solid organ injury and rupture of an abdominal aortic aneurysm are two common causes of rapid internal blood loss. Finally, hypovolemic shock can result from significant fluid (other than blood) loss. Two examples of hypovolemic shock secondary to fluid loss include refractory gastroenteritis and extensive burns. The remainder of this chapter will concentrate mainly on hypovolemic shock secondary to blood loss and the controversies surrounding the treatment of this disease. The reader is referred to other chapters in this text for discussions of the pathophysiology and treatment for hypovolemic shock resulting from fluid losses other than blood.

The many life-threatening injuries suffered during the wars of the 1900's have significantly impacted the development of the principles of hemorrhagic shock resuscitation. During W.W.I, W.B. Cannon recommended delaying fluid resuscitation until the cause of the hemorrhagic shock was surgically repaired. Crystalloid and blood were used extensively during W.W.II for the treatment of unstable patients.

Pathophysiology: The human body responds to acute hemorrhage by activating four major physiologic systems: the hematologic system, the cardiovascular system, the renal system and the neuroendocrine system.

The hematologic system responds to an acute severe blood loss by activating the coagulation cascade and contracting the bleeding vessels (via local thromboxane A2 release). In addition, platelets are activated (also via local thromboxane A2 release) which form an immature clot on the bleeding source. The damaged vessel exposes collagen, which subsequently causes fibrin deposition and stabilization of the clot. Approximately 24 hours are needed for complete clot fibrination and mature formation.

The cardiovascular system initially responds to hypovolemic shock by increasing the heart rate, increasing myocardial contractility and constricting peripheral blood vessels. This response occurs secondary to an increase in release of norepinephrine and a decrease in baseline vagal tone (regulated by the baroreceptors in thecarotid arch, aortic arch, left atrium and pulmonary vessels). The cardiovascular system also responds by redistributing blood to the brain, heart and kidneys and away from skin, muscle and the gastrointestinal tract.

The kidneys respond to hemorrhagic shock by stimulating an increase in renin secretion from the juxtaglomerular apparatus. Renin converts angiotensinogen to angiotensin I, which is subsequently converted to angiotensin II by the lungs and liver. Angiotensin II has two main effects, both of which help reverse hemorrhagic shock: vasoconstriction of arteriolar smooth muscle and stimulation of aldosterone secretion by the adrenal cortex. Aldosterone is responsible for active sodium reabsorption and subsequent water conservation.

The neuroendocrine system responds to hemorrhagic shock by causing an increase in circulating antidiuretic hormone (ADH). ADH is released from the posterior pituitary gland in response to a decrease in blood pressure (as detected by baroreceptors) and a decrease in sodium concentration (as detected by osmoreceptors). ADH indirectly leads to an increase in reabsorption of water and salt (NaCl) by the distal tubule, collecting ducts and the loop of Henle.

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• Symptoms of shock such as weakness, lightheadedness, and confusion should be determined in all patients.

• In the trauma patient, one should determine the mechanism of injury and any information that may heighten suspicion of certain injuries (e.g., steering wheel damage, extensive passenger compartment intrusion in a motor vehicle accident).

• If conscious, the patient may be able to indicate the location of pain.

• Vital signs prior to arrival should also be noted.

• Vascular disorders may present with chest, abdominal or back pain.

• The classic history of a thoracic aneurysm is a tearing pain, radiating through to the back. Abdominal aortic aneurysms usually present with abdominal or back pain.

• For gastrointestinal (GI) bleeding, one should inquire about hematemesis, melena, any drinking history, excessive NSAID use or any coagulopathies (iatrogenic or otherwise).

• The chronology of vomiting and hematemesis should also be determined.

• The patient who presents with hematemesis after multiple episodes of forceful vomiting is more likely to have Boerhaave's syndrome or a Mallory-Weiss tear, whereas a history of hematemesis from the start is more consistent with peptic ulcer disease or esophageal varices.
  
• If a gynecologic cause is considered, information that should be obtained includes the last menstrual period, risk factors for ectopic pregnancy, vaginal bleeding (including amount and duration), vaginal passage of products of conception and any pain. Note that all women of child-bearing age should have pregnancy ruled out with a pregnancy test, regardless of whether they believe they could be pregnant.

• Class I Hemorrhage (Loss of 0-15%):

• In the absence of complications, only minimal tachycardia will be seen.

• There are usually no changes in blood pressure, pulse pressure or respiratory rate.

• A delay in capillary refill of greater than three seconds corresponds to approximately a 10% volume loss.

• Class II Hemorrhage (Loss of 15-30%):

• Clinical symptoms include tachycardia > 100 bpm, tachypnea, decrease in pulse pressure, cool clammy skin, delayed capillary refill and slight anxiety.

• The decrease in pulse pressure is a result of increased catecholamines causing an increase in peripheral vascular resistance and a subsequent rise in the diastolic blood pressure.

• Class III Hemorrhage (Loss of 30-40%):

• By this point, patients usually have marked tachypnea and tachycardia, a fall in systolic blood pressure, oliguria and significant changes in mental status, such as confusion or agitation.

• In patients without other injuries or fluid losses, this is the smallest amount of blood loss that consistently causes a fall in systolic blood pressure.

• Most of these patients will require blood transfusions, but this decision should be made based on initial response to fluids.

• Class IV Hemorrhage (Loss of > 40%):

• Symptoms include: marked tachycardia, decreased systolic blood pressure, narrowed pulse pressure (or immeasurable diastolic pressure), markedly decreased (or no) urinary output, depressed mental status (or loss of consciousness) and cold and pale skin.

• This amount of hemorrhage is immediately life-threatening.

• In the trauma patient, hemorrhage is usually the presumed cause of shock. However, it must be distinguished from other causes of shock. These include cardiac tamponade (muffled heart tones, distended neck veins), tension pneumothorax (deviated trachea, unilaterally decreased breath sounds), and spinal cord injury (warm skin, lack of expected tachycardia, and neurological deficits).

• There are four areas where one can sustain life-threatening hemorrhage: the chest, the abdomen, the thighs and externally (the floor).

• The chest should be auscultated for decreased breath sounds, as life-threatening hemorrhage can occur from myocardial, vessel or lung laceration.
  
  The abdomen should be examined for tenderness or distension, which may indicate intraabdominal injury.

• The thighs should be checked for deformities or enlargement (signs of femur fracture and bleeding into the thigh).
  
  The entire patient should then be checked for any external bleeding.
  
• In the atraumatic patient, the majority of hemorrhage will be in the abdomen. The abdomen should be examined for tenderness, distension, or bruits. Look for evidence of an aortic aneurysm, peptic ulcer disease or liver congestion. Also check the patient for other signs of bruising or bleeding.
  
• In the pregnant patient, one should perform a sterile speculum examination. This is with the exception of third trimester bleeding where the examination should be done as a "double set-up" in the operating room. Check for abdominal, uterine or adnexal tenderness

• Traumatic causes can result from penetrating and blunt trauma. Common traumatic injuries which can result in hemorrhagic shock include: myocardial laceration and rupture, major vessel laceration, solid abdominal organ injury, pelvic and femur fractures and scalp lacerations.

• Vascular disorders, which can result in significant blood loss, include aneurysms, dissections and arteriovenous malformations.

• Examples of gastrointestinal disorders, which can result in hemorrhagic shock, include: bleeding esophageal varices, bleeding peptic ulcers, Mallory-Weiss tears and aorto-intestinal fistulas.

• Pregnancy-related disorders include ruptured ectopic pregnancy, placenta previa and abruption of the placenta.

• Initial laboratory studies should include a complete blood count (CBC), electrolytes (e.g., Na, K, Cl, HCO3, BUN, creatinine, glucose), prothrombin time (PT), partial thromboplastin time (PTT), type and crossmatch, arterial blood gas (ABG) and a urinalysis (in trauma patients).

• Markedly hypotensive/unstable patients must be first adequately resuscitated. This takes precedence over imaging studies, and may include immediate interventions and/or being rushed immediately to the operating room.

The work-up of the trauma patient who presents with signs and symptoms of hypovolemia is directed toward finding the source of blood loss.

The atraumatic patient who presents in hypovolemic shock will require an ultrasound in the emergency department if an AAA is suspected. If gastrointestinal bleeding is suspected, the patient will need to have a nasogastric tube placed and gastric lavage performed. Upright CXR should be obtained if a perforated ulcer or Boerhaave's syndrome is a possibility. Endoscopy can be performed to further delineate the source of bleeding (usually after the patient has been admitted).

All female patients of child bearing years should have a pregnancy test done. If the patient is pregnant and in shock, a pelvic US should be performed immediately in the emergency department. A culdocentesis may be performed, although in most places, ultrasound can be done in the ED, and yields more information on the source of bleeding.

• If thoracic dissection is suspected by mechanism and initial chest x-ray, the work up may include transesophageal echocardiography, aortography or computerized tomography (CT) of the chest.

• If abdominal injury is suspected, diagnostic peritoneal lavage (DPL) may be performed in the unstable patient or CT scan in the stable patient.

• An increasing role for ultrasound is emerging, although not yet as sensitive as DPL or CT scan.
  
• If long bone fractures are suspected, radiographs should be obtained.

 

There has been considerable debate, in recent years, over the use of military antishock trousers (MAST). MAST were introduced in the 1960's and, based mostly on anecdotal reports of success, they became standard therapy in the prehospital treatment of hypovolemic shock in the late 1970's. By the 1980's the American College of Surgeons Committee on Trauma had made them the standard of care for all trauma patients with signs or symptoms of shock. Since that time, studies have failed to show improved outcome with the use of MAST. Current recommendations by the American College of Surgeons Committee on Trauma call for the use of MAST for 1) the splinting of pelvic fractures in cases of continuing bleeding and hypotension, and 2) for intra-abdominal trauma in patients with severe hypovolemia, who are in route to definitive care. Contraindications include pulmonary edema, diaphragmatic rupture, and uncontrolled hemorrhage outside of the confines of the garment.

• There has been much discussion and research on whether crystalloids or colloids are best for resuscitation. Many fluids have been studied for resuscitation including NS, LR, hypertonic saline, albumin, purified protein fraction (PPF), fresh frozen plasma (FFP), Hetastarch (HES), Pentastarch (PES) and dextran 70.

• Proponents of colloid resuscitation argue that the increased oncotic pressure offered by these substances will decrease pulmonary edema. The pulmonary vasculature, however, allows considerable flow between the intravascular space and interstitium (including proteins). Maintenance of pulmonary hydrostatic pressure below 15 mm Hg appears to be a much larger factor in preventing pulmonary edema.

 

• The combination of hypertonic saline and dextran (HSD) has also been studied because of some previous evidence that it may improve cardiac contractility and circulation. Studies in the United States and Japan have failed to show any difference when compared with NS or LR.

• Thus, despite the many types of resuscitation fluid available, current recommendations still advocate the use of NS or LR.

• Another area of interest with regard to resuscitation is whether or not the goal should be to restore normal circulating volume and blood pressure prior to definitive control of bleeding.

• Cannon, during World War I, observed and characterized patients in clinical shock. He later suggested a model of permissive hypotension in the treatment of torso wounds with the intent of minimizing further bleeding.

 

• Since then, many studies have been done trying to determine if these principles are valid in patients with uncontrolled hemorrhage. The majority of these studies show increased survival in the permissive hypotension or delayed treatment arms. The theory is that increased pressure will cause more bleeding and disrupt initial clots, whereas extreme hypotension may risk cerebral perfusion.

 

Complications:

• Neurologic sequelae

• Death

Prognosis:

• The prognosis is dependent on the degree of volume loss.

• A very common error in the management of hypovolemic shock, is failure to recognize it early.

• This leads to delay in diagnosing the cause and in resuscitating the patient.

• This often happens due to a reliance on blood pressure or initial hematocrit, rather than signs of decreased peripheral perfusion, in order to make the diagnosis.

• Missed injuries in trauma patients can occur, especially if the examining physician focuses on more obvious injuries. This can be avoided by being sure to complete the physical examination and by continuing to monitor the patient closely and performing repeated examinations.

• The elderly tolerates hypovolemia less well. Aggressive therapy should be instituted early to avoid potential complications such as myocardial infarction and stroke.

• In patients who require large amounts of volume resuscitation, care should be taken to avoid hypothermia as this can contribute to developing an arrhythmia or coagulopathy. This can be avoided by warming the IV fluids prior to administration.

• Patients on beta blockers, calcium channel blockers, and those with pacemakers may not mount a tachycardic response to hypovolemia leading to a delay in the diagnosis of shock. To minimize this, all patients histories should include medications and the examiner should rely on other signs of decreased peripheral perfusion.

• Coagulopathies can occur in patients receiving large amounts of volume resuscitation. This is due to dilution of platelets and clotting factors but is rare within the first hour of resuscitation. Baseline coagulation studies should be drawn and should guide the administration of platelets and fresh frozen plasma (FFP).