Introduction
Hypovolemic shock is an emergency condition where the cardiac output is insufficient for general body requirement. The heart is unable to pump enough blood due to severe blood and intravascular fluid loss. It causes multi-organ failure hence involvement of all body systems. It is majorly caused by “bleeding from injuries, cuts and internal occult bleeding, such as the gastrointestinal tract” (Heller, 2010, p. 1). Conditions such as burns, diarrhea, excessive perspiration and vomiting may also lead to hypovolemic shock. Dehydration is a major cause in pediatric age group. The pathophysiology describes the mechanism of the shock and relates it to the presentation which is multi-systemic.
The severity depends on the amount and duration of blood loss. There is early presentation and rapid blood loss while severity increases with increased amount lost. This makes hypovolemic shock a medical emergency that requires immediate intervention. The understanding of its pathophysiology is relevant in description of the various signs and symptoms and deranged tests. It is also important in formulating appropriate intervention and management measures for the patient (Heller, 2010).
Presentation Symptoms
The patient is usually anxious or agitated initially. His/her skin becomes clammy and cold. Confusion sets in and patient feels general body weakness. With continued blood loss, patient becomes thirsty, has decreased or no urine output. He develops severe pallor and the skin become moist due to sweating. The patient then goes into coma with loss of consciousness. The greater and more fast the intravascular fluid loss, the more severe the symptoms become (Anon, n.d.).
Other systems involved include respiratory system where the patient experiences weak, rapid and labored respiration. The patient may have chest pains and in complicated cases, may show respiratory features of congestive cardiac failure. Cardiovascular features include bounding, rapid pulse, severe sweating and shortness of breath. He complains of abdominal pain and feels thirsty. The patient also manifests with anuria/oliguria. There is generalized body weakness and fatigue. Chronic blood loss may also manifest with bone pain (Anon, 2006).
Signs
The hallmark clinical indicators of shock are the presence of altered vital signs; there is tachycardia, oliguria and altered mental status. The finding indicates secondary effects of circulatory failure, not the primary causative event. Due to age, use of particular medication, some hypotensive patients might present with normal pulse and arterial pressures. The clinical signs also depend on severity and duration of blood loss. The signs are majorly per system summing up into a constellation.
On general examination, the patient has severe pallor. May or may not have central cyanosis. Initially, the patient looks agitated, becomes confused and may become unconscious if bleeding continues. Since the condition is acute, there should be no wasting of time. The vitals are always derenched. The skin may be pale, ash-like, and usually with diaphoresis. Inspection for paleness on the palpebral conjunctivae usually gives negative results, for it is a sign of chronic anemia.
The patient is tachypnoeic with a respiratory rate of more than 30 breaths per minute and usually labored. This is a deviation from the reference value of about 16-18 breaths per minute. He/she usually has tachycardia, absent/ weak peripheral pulses. The pulse rate is far much above reference values of 60-100 beats per minute. The blood pressure is less than 115 systolic and 80 diastolic with normal average blood pressure being 120/80.
In the cardiovascular system, you find weak/absent peripheral pulses, tachycardia and reduced blood pressures. There may be chest pains. There is palpitation and heaves. A systolic murmur may be heard. The patient may be tachypnoiec and in labored breathing. He complains of chest pains and tenderness. The chest is percussed and auscultated for hemothorax. There will be reduced breath sounds and dull percussion note on the side of bleeding.
Abdominal tenderness may be manifested. On further examination, the cause of the bleeding may be found, which may be internal or external. Signs of intra-abdominal hemorrhage would include distended abdomen, tenderness and dullness on percussion. The flanks are also examined for ecchymosis, which indicate retroperitoneal hemorrhage. Examination for ruptured abdominal aortic aneurysms may include palpable pulsatile mass in the abdomen, scrotal enlargement due to retroperitoneal blood tracking, mottling of lower extremity, and diminished femoral pulses. The rectum is inspected for hemorrhoids especially in patients with portal hypertension.
A full pelvic exam is required for patients with a history of vaginal bleeding. Pregnancy test is done to rule out ruptured ectopic pregnancy. Trauma patient (like in this case scenario) are approached systematically. The principal of primary and secondary examination is used. The primary examination is a quick maneuver that is used to identify life-threatening problems. Airway is assessed if patent. Oropharynx is examined for blood or foreign materials. The neck is inspected for tracheal deviation or hematomas. The lungs are auscultated and percussed to rule out hemothorax or pneumothorax. Radial and femoral pulses are palpated for rate, volume and rhythm. A quick external inspection is done for any external bleeding. A gross nervous system is done and level of consciousness determined (AVPU). Patient is then exposed fully; thermoregulation is maintained with warm coverings and external heat source.
The secondary examination is majorly head to toe. The examination is done carefully and it attempts to find all injuries (Udeani and Geibel, 2011). Thorough history taking and physical findings may be vital in identifying the cause and planning appropriate means of management (Theodore and Burton, 2011).
Causes
Hypovolemic shock is due to loss of both circulating blood volume and oxygen carrying capacity. Penetrating and blunt trauma, gastrointestinal bleeding, and obstretical bleeding are among the commonest clinical etiologies.
Pathophysiology
Trauma is one of the frequent causes of hypovolemia. The blood loss estimates following fractures, stab wounds and accident (road traffic accidents) rate high as major contributors of hypovolemic shock. Bleeding leads to reduction in volume of circulating blood. This leads to reduced venous return. Reduced venous return cascades to reduce preload and therefore reduced ejection volume, and hence reduced cardiac output. Compensatory systemic release of catecholamine (noradrenaline, adrenaline and dopamine) leads to peripheral vessels vasoconstriction, increased myocardial contractility and increased pulse rate. It has been noted that these “compensatory mechanisms are aimed at improving the compromised cardiac output” (Stickler, 2010, p. 1). It should further be noted that:
Systemic blood pressure may therefore remain stable in the face of persistent hypovolemia. Increased pulse rate (tachycardia) promotes increased myocardial oxygen demand that, together with compromised tissue perfusion, may result in cardiac failure. Finally, anaerobic metabolism that occurs due to impaired perfusion may lead to metabolic acidosis, which together with the myocardial dysfunction contributes to multi-organ failure. (Stickler, 2010, p. 1)
Ten percent loss of total blood volume may present with no effect on cardiac output and arterial pressure. The following should be noted:
- Blood loss of more than 10% leads to diminished cardiac output due to decreased preload; this leads to reduced oxygen delivery to tissues. Blood loss of more than 20% of total blood volume leads to decline in arterial pressure. Hypotension and hypovolemia exert differential effects on organ function. (Kreimeier, 2000, p. 1)
There is increased adrenergic activity in splanchic organs, and these organs are highly vulnerable in patients with hypovolemic shock and hypotension. Due to diminished gastrointestinal perfusion, ischemia develops; especially the mucosal layer leading to its integrity being compromised.
- Impaired gut barrier function may allow entry bacteria and endotoxins to general circulation hence precipitation of systemic septicemia as a consequence of shock. However, the splanchic organs are refractory to the effects of intravenous administered fluids. (Kreimeier, 2000, p. 1)
There is also redistribution of blood of flow away from non-vital organs – skin, GIT, and kidneys. These explain for cold-clammy skin, abdominal tenderness and oliguria/anuria. There is also concurrent hormonal response to acute hemorrhage. Corticotrophin-release hormone is directly stimulated. This leads to release of beta-endorphin and glucocorticoid. Vasopressin is also released causing water retention at distal tubules. The juxtamedullary complex releases rennin in response to decreased arterial pressure. Renin leads to increased aldosterone levels that are responsible for sodium and water re-absorption. There is increased production of glucagon and growth hormone that are responsible for the hyperglycaemia in acute hemorrhage. Insulin is also inhibited by circulating catecholamines.
In addition, there are organ specific changes that occur. The brain has a good auto regulation of cerebral blood flow. It can tolerate a wide range of systemic arterial blood pressure. If this is exceeded, coma sets in. kidneys can tolerate a large decrease in arterial pressure for only shot duration. Renal failure occurs in persistent states. Early and appropriate intervention may avert organ damage. However, it is clear that the reduced vascular volume is responsible for the reduced arterial pressure despite presence of vasoconstrictors. There may be decompensation changes if the hypovolemia is not corrected on time (Udeani & Geibel, 2011).
Diagnostic Tests
Laboratory work-ups may not be helpful in acute hemorrhagic shock since values do not change until there is redistribution of interstitial fluid into vascular space that occurs after 8-12 hours. Many of the derangement are due to over-zealous resuscitation with fluids or blood products. Hemoglobin and hematocrit remains normal immediately after blood loss. Hematocrit usually falls during the course of resuscitation secondary to crystalloid infusion on re-equilibration of extracellular fluid into the vascular space. A hemoglobin concentration of less than 7g/dl in acute patient may necessitate blood transfusion as there is high chance of further fall.
Blood gas analysis is of great significance. pH of 7.30-7.35 is abnormal but tolerable in acute state. Metabolic acidosis signifies presence of tissue hypoxia. pH of less than 7.2 indicates life threatening academia hence need for aggressive resuscitation. Avoid exogenous bicarbonate but of help in severe acidemia.
Prothrombin time (PT), activated partial thromboplastin time (aPTT) can be measured. Bleeding time (BT) can be done to evaluate platelet function. Electrolyte studies usually are of significant value especially after massive resuscitation with crystalloids. Sodium and chloride levels may increase with administration of large volumes of isotonic sodium chloride. Calcium levels decrease with large volumes of IV fluids or rapid transfusion, which is secondary to chelation of calcium by EDTA in stored blood. Potassium levels may also increase with transfusion of large volumes of blood.
Renal function test are of significant importance. Creatinine and blood urea are usually abnormal of renals are involved. Always remember a blood sample for blood group and cross-match as soon as the patient arrives. 4 units of blood should always be prepared for actively bleeding patient (Udeani and Geibel, 2011).
Imaging studies are usually directed at finding the cause. They may include x-rays, U/S, CT scan and MRI. Chest x-rays may show diagnosis of hemothorax by showing a large opacity. Hemothoracex diagnosed as complete whiteout of pleural space. Computed tomography (CT) scan is very sensitive and specific for identifying intrathoracic, intraabdominal and retroperitoneal hemorrhage. Ultrasound is often chosen for diagnosing bleeding into cavities, though it is limited in its ability to evaluate retroperitoneal space. U/S is cheaper and readily available, plus has no radiation complication (McCance & Huether, 2010).
Esophagogastroduodenoscopy (EGD) is the test of choice for upper gastrointestinal bleeding. It provides additional therapeutic advantage. Colonoscopy is used in lower gastrointestinal bleeding. Focused abdominal sonographic technique (FAST), is the investigation of choice in identification of intraperitoneal fluid in trauma patients with hemorrhage. Angiography is used in investigation of acute hemorrhage from multiple various sources. Nuclear medicine scanning is used to localize gastrointestinal bleeding (Udeani & Geibel, 2011).
Procedures
Bedside diagnostic peritoneal lavage is helpful in determining if there is significant injury to underlying structures or intra-abdominal bleeding. If more than 5ml of blood is aspirated, laparatomy is usually indicated. Central venous access is considered an adjunct to peripheral intravenous lines. Large bore (12F) central resuscitation lines are preferred. Hemothorax is managed by drainage by insertion of large caliber chest tube, or open thoracotomy. Thoracotomy is preferred in the presence of persistent bleeding.
Management
Controlling the bleeding and replacing the fluids should be quickly carried out. Fluid replacement is aimed at normalizing of hemodynamic parameters. This is especially relevant when the source of bleeding is already managed. In cases where “bleeding is stopped due to hypotension, vasoconstriction and clot formation, fluid replacement is directed to restoration or radial pulse or restoration of sensorium or obtaining a blood pressure of 80mmHg” (Kreimeier, 2000, p. 1). This is achieved by giving 250 ml of Ringer’s lactate solution (hypotensive resuscitation).
Management is also based on duration of evacuation time. When the evacuation time is less than 1 hour, immediate evacuation to surgical centre is indicated. Introducing intravenous line is suspended till the patient arrives at the surgical facility. Resuscitation should be done together or before any diagnostic studies.
Crystalloids are the first fluid of choice for resuscitation of these patients. 2 liters of isotonic sodium chloride solution or Ringer’s lactate is immediately administered in response to hypovolemic shock from blood loss. Fluid replacement is continued until stabilization of patient’s hemodynamics. Each litre of fluid expands blood volume by 20-30% as crystalloids easily leak from vascular space; i.e 3 liters of fluid are administered to raise blood volume by 1 liter (Craft, Gordon & Tiziani, 2011).
Colloids restore volume in the ratio 1:1. Examples include human albumin, hydroxyethyl starch products, or hypertonic saline dextran combinations. Large volumes (more than 1500ml/day) of hydroxyethyl starch products mixed in 0.9% isotonic sodium chloride solution is associated with induction of coagulopathy and is therefore routinely avoided (Hudson, 2009). Blood is only administered or transfused if after 2 liters of crystalloid resuscitation the patient still remains unstable. O-negative cross matched blood is preferred in acute states. Start group specific blood as soon as it is available. Fresh frozen plasma is infused if patient shows signs of coagulopathy (Miyajima et al., 2010).
Surgery may be considered to control the bleeding and in complicated cases. Note that consultation with hematologist is of essential significance. Gynaecological team may be called in action in situation of per vaginal bleeding.
Follow-up
The remainder of management and care will be determined by proximate course of the hypovolemic shock. These patients with hypovolemia may complicate with acute tubular necrosis of the renals, acute lung injury, transfusion-related acute lung injury, infections, and multiple organ dysfunction syndromes, with its attendant risk of death. Erythropoietin(40000 U/week, together with hematinics (iron and folate supplements) and vitamin C are helpful in boosting hemopoesis in acute setting when bone marrow is unable to mount the response (Craft, Gordon & Tiziani, 2011).
Complications and Prognosis
Death is the primary complication of hemorrhagic shock, majorly due to poor and late intervention measures. Resuscitation may be responsible for the spectrum of organ failure; overzealous resuscitation measures. The cascade of systemic inflammatory syndrome (SIRS) leading to multiple organ failure syndrome complicates about 30-70% of patient with hypovolemic shock due hemorrhage and survive initial fluid resuscitation.
Prognosis depends on ability to resuscitate and the sort of injury. Presentation of the hemorrhage or hypovolemic shock does not determine prognosis (Udeani & Geibel, 2011).
Conclusion
Proper management and resuscitation of a patient in hypovolemic shock is of utmost importance. The understanding of the causes, presentation, pathophysiology and relevant diagnostic tests is critical in the formulation of management plan of the patient. The physiological changes assists the clinicians to understand why the presentation and assists in interpreting the abnormal vitals and lab findings. It should also be emphasized of the role of over-zealous resuscitation measures on the pathophysiology of hypovolemic shock. The risk of metabolic acidosis and congestive cardiac failure requires no further highlight. It should be realized that trauma from stab wounds may present with occult bleeding into internal viscera hence proper history and examination are of critical importance. Patients with hypovolemic shock due to hemorrhage are at risk of complication in each and every system, with its attendant risk of death. Patient’s education is of significant utility.
References
Anon. (2006). Ambulance technician study-shock. Ambulancetechnicianstudy. Web.
Anon. (n.d.). Hypovolemic Shock. Mdguidelines. Web.
Craft, A. Gordon, C. & Tiziani, A. (2011). Understanding Pathophysiology (1st ed.). Sydney: Mosby.
Heller, J. (2010). Hypovolemia shock. NLM.NIH. Web.
Heller, J. (2011). Hypovolemic shock. emedicine.
Hudson, K. (2009). Hypovolemia shock- 1 nursing CE. Dynamicnursingeducation. Web.
Kreimeier, W. (2000). Pathophysiology of fluid imbalance. Biomedcentral.
McCance, K. L. & Huether, S. E. (2010). Pathophysiology: the biologic basis for disease in adults and children (6thEdition). Maryland Heights: Mosby Elsevier.
Miyajima et al. (2010). Massive gastric bleeding from blunt abdominal trauma: report of a case. hinari.gw.who.int . Web.
Stickler, J. (2010). Traumatic hypovolemic shock: Halt the downward spiral. journals.lww.
Theodore, P & Burton, A. (2011). Clinical manifestation and diagnosis of volume depletion in adults.uptodate.
Udeani, J & Geibel, C. (2011). Hemorrhagic shock, clinical presentation. emedicine. Web.