shock

shock is a condition of reduced tissue perfusion, resulting in the inadequate

delivery of oxygen and nutrients that are necessary for cellular function.

Definition:

On a multicellular level, the definition of shock becomes more difficult because not all tissues and organs will experience the same amount of oxygen imbalance for a

given clinical disturbance.

Hypovolemic Vasogenic (septic) Cardiogenic Neurogenic

The 4 classes of shock, as proposed by Alfred Blalock, are as follows

A cut loss of circulating blood volume.

The risk factor for hemorrhagic shock:

Pt age. Severity of injury with anatomical postion. Time lapse between injury and intiation of

treatment. Prehospital fluid therapy & application of PACG. Medication used for chronic condition

Hemorrhage:

CLASS I CLASS II CLASS III CLASS IV

Blood loss(ml)

Up to750 750-1500 1500-2000 >2000

Blood loss %

15% 15%-30% 30%-40% >40%

Pulse rate <100 100-120 120-140 >140

BP N N dec dec

P. pressure N or incr dec dec dec

R.R 14-20 20-30 30-40 >35

U.O.P >30 20-30 5-15 negligble

CNS Sligh anxi Mildly anxi Anxi ,conf Conf,letharg

Fluid replac crystalloid crystalloid Cryst,blood Cryst,blood

the most common type, results from a loss of circulating blood volume from clinical etiologies, such as penetrating and blunt trauma, gastrointestinal bleeding, and obstetrical bleeding.

Humans are able to compensate for a significant hemorrhage through various neural and hormonal mechanisms.

Hypovolemic shock

these responses act to systematically divert circulating volume away from non vital organ systems so that blood volume may be conserved for vital organ function.

Acute hemorrhage causes a decreased cardiac output and decreased pulse pressure.

Pathophysiology

These changes are sensed by baroreceptors in the aortic arch and atrium.

With a decrease in the circulating volume, neural reflexes cause an increased sympathetic outflow to the heart and other organs.

The response is an increase in heart rate, vasoconstriction, and redistribution of blood flow away from certain non vital organs, such as the skin, gastrointestinal tract, and kidneys.

a multisystem hormonal response to acute hemorrhage occurs.

Corticotropin-releasing hormone is stimulated directly. This eventually leads to glucocorticoid and beta-endorphin release.

Vasopressin from the posterior pituitary is released, causing water retention at the distal tubules.

Renin is released by the juxtamedullary complex in response to decreased mean arterial pressure, leading to increased aldosterone levels and eventually to sodium and water resorption.

Hyperglycemia commonly is associated with acute hemorrhage.

This is due to a glucagon and growth hormone–induced increase in gluconeogenesis and glycogenolysis.

Circulating catecholamines relatively inhibit insulin release and activity, leading to increased plasma glucose.

In addition to these global changes, many organ-specific responses occur.

The brain has remarkable autoregulation that keeps cerebral blood flow constant over a wide range of systemic mean arterial blood pressures.

The kidneys can tolerate a 90% decrease in total blood flow for short periods of time.

With significant decreases in circulatory volume, intestinal blood flow is dramatically reduced by splanchnic vasoconstriction.

Early and appropriate resuscitation may avert damage to individual organs as adaptive mechanisms act to preserve the organism.

Hemorrhagic shock is tolerated differently, depending on the preexisting physiologic state and, to some extent, the age of the patient.

Very young and very old people are more prone to early decompensation after loss of circulating volume.

Age

Pediatric patients have smaller total blood volumes and, therefore, are at risk to lose greater percentage of blood on an equivalent-volume basis during exsanguination compared to adults.

The kidneys of children younger than 2 years are not mature; they have a blunted ability to concentrate solute.

Younger children cannot conserve circulating volume as effectively as older children.

Also, the body surface area is increased relative to the weight, allowing for rapid heat loss and early hypothermia, possibly leading to coagulopathy.

Elderly people may have both altered physiology and preexisting medical conditions that may severely impair their ability to compensate for acute blood loss.

Atherosclerosis and decreased elastin cause arterial vessels to be less compliant, leading to blunted vascular compensation, decreased cardiac arteriolar vasodilation, and angina or infarction when myocardial oxygen demand is increased.

Older patients are less able to mount a tachycardia in response to decreased stroke volume because of decreased beta-adrenergic receptors in the heart and a decreased effective volume of pacing myocytes within the sinoatrial node.

Also, these patients frequently are treated with a variety of cardiotropic medications that may blunt the normal physiological response to shock.

These include beta-adrenergic blockers, nitroglycerin, calcium channel blockers, and antiarrhythmics.

The kidneys also undergo age-related atrophy, and many older patients have significantly decreased creatinine clearance in the presence of near-normal serum creatinine.

Concentrating ability may be impaired by a relative insensitivity to antidiuretic hormone.

These changes in the heart, vessels, and kidneys can lead to early decompensation after blood loss.

All of these factors in concert with comorbid conditions make management of elderly patients with hemorrhage quite challenging.

The most common clinical etiologies are penetrating and blunt trauma, gastrointestinal bleeding, and obstetrical bleeding.

Causes

History:

-No single historical feature is diagnostic of shock. Some patients may report fatigue, generalized lethargy, or lower back pain (ruptured abdominal aortic aneurysm).

- Others may arrive by ambulance or in the custody of law enforcement for the evaluation of bizarre behavior.

Clinical

Obtaining a clear history of the type, amount, and duration of bleeding is very important.

Many decisions in regard to diagnostic tests and treatments are based on knowing the amount of blood loss that has occurred over a specific time period.

If the bleeding occurred at home or in the field, an estimate of how much blood was lost is helpful.

For GI bleeding, knowing if the blood was per rectum or per os is important. Because it is hard to quantitate lower GI bleeding, all episodes of bright red blood per rectum should be considered major bleeding until proven otherwise.

Bleeding because of trauma is not always identified easily.

The pleural space, abdominal cavity, mediastinum, and retroperitoneum are all spaces that can hold enough blood to cause death from exsanguination.

External bleeding from trauma can be significant and can be underestimated by emergency medical personnel.

Multiple open fractures can lead to the loss of several units of blood.

Scalp lacerations are notorious for causing large underestimated blood loss.

The physical examination in patients with hemorrhagic shock is a directed process.

Often, the examination will be paramount in locating the source of bleeding and will provide a sense of the severity of blood loss.

Physical

The hallmark clinical indicators of shock have generally been the presence of abnormal vital signs, such as hypotension, tachycardia, decreased urine output, and altered mental status.

These findings represent secondary effects of circulatory failure, not the primary etiologic event

Because of compensatory mechanisms, the effects of age, and use of certain medications, some patients in shock will present with a normal blood pressure and pulse.

The general appearance of a patient in shock can be very dramatic. The skin may have a pale & usually with diaphoresis.The patient may appear confused or agitated and may become obtunded.

• The pulse first becomes rapid and then becomes dampened as the pulse pressure diminishes. Systolic blood pressure may be in the normal range during compensated shock.

• The conjunctivae are inspected for paleness, a sign of chronic anemia. The nose and pharynx are inspected for blood.

• The chest is auscultated and percussed to evaluate for hemothorax. This would lead to loss of breath sounds and dullness to percussion on the side of bleeding.

The abdominal examination searches for signs of intra-abdominal bleeding, such as distention, pain with palpation, and dullness to percussion.

The flanks are inspected for ecchymosis, a sign of retroperitoneal bleeding. Ruptured aortic aneurysms are one of the most common conditions that cause patients to present in unheralded shock.

Signs that can be associated with a rupture are a palpable pulsatile mass in the abdomen, scrotal enlargement from retroperitoneal blood tracking, lower extremity mottling, and diminished femoral pulses.

• The rectum is inspected. If blood is noted, take care to identify internal or external hemorrhoids. On rare occasion, these are a source of significant bleeding, most notably in patients with portal hypertension.

• Patients with a history of vaginal bleeding undergo a full pelvic examination. A pregnancy test is warranted to rule out ectopic pregnancy.

Trauma patients are approached systematically, using the principles of the primary and secondary examination.

Trauma patients may have multiple injuries that need attention concurrently, and hemorrhage may accompany other types of insults, such as neurogenic shock.

◦ To assess the airway, ask the patient's name. If the answer is articulated clearly, the airway is patent.

◦ The oral pharynx is inspected for blood or foreign materials.

◦ The neck is inspected for hematomas or tracheal deviation.

The primary survey is a quick maneuver that attempts to identify life-

threatening problems.

◦ The lungs are auscultated and percussed for signs of pneumothorax or hemothorax.

◦ The radial and femoral pulses are palpated for

strength and rate. ◦ A quick inspection is made to rule out any external

sources of bleeding.

◦ A gross neurological examination is performed by asking the patient to squeeze each hand and dorsiflex both feet against pressure.

◦ The patient then is exposed completely, taking care to

maintain thermoregulation with blankets and external warming devices.

◦ The scalp is inspected for bleeding. Any active bleeding from the scalp should be controlled before proceeding with the examination.

◦ The mouth and pharynx are examined for blood.

The secondary examination is a head-to-toe, careful examination that attempts to identify all injuries.

◦ The abdomen is inspected and palpated.

Distention, pain on palpation, and external ecchymosis are indications of intra-abdominal bleeding.

◦ The pelvis is palpated for stability. Crepitus or

instability may be an indication of a pelvis fracture, which can cause life-threatening hemorrhage into the retroperitoneum.

Long bone fractures are noted by localized pain to palpation and boney crepitus at the site of fracture. All long bone fractures should be straightened and splinted to prevent ongoing bleeding at the sites.

Femur fractures are especially prone to large blood losses and should be immobilized immediately in a traction splint.

Laboratory Studies:

laboratory values are not helpful in acute hemorrhage because values do not change from normal until redistribution of interstitial fluid into the blood plasma occurs after 8-12 hours.

Workup

Hemoglobin and hematocrit values remain unchanged from baseline immediately after acute blood loss.

During the course of resuscitation, the hematocrit may fall secondary to crystalloid infusion and re-equilibration of extracellular fluid into the intravascular space.

• No absolute threshold hematocrit or hemoglobin level that should prompt transfusion exists. A hemoglobin concentration of less than 7 g/dL in the acute setting in a patient that was otherwise healthy is concerning only because the value most likely will drop considerably after re-equilibration.

• In the absence of preexisting disease, transfusions can be withheld until significant clinical symptoms are present or the rate of hemorrhage is enough to indicate ongoing need for transfusion.

• Patients with significant heart disease are at higher risk of myocardial ischemia with anemia, and transfusion should be considered when values drop below 7 mg/dL.

Arterial blood gas may the most important laboratory value in the patient in severe shock.

• Acidosis is the best indicator in early shock of ongoing oxygen imbalance at the tissue level. A blood gas with a pH of 7.30-7.35 is abnormal but tolerable in the acute setting.

• The mild acidosis helps unload oxygen at the peripheral tissues and does not interfere with hemodynamics.

A pH below 7.25 may begin to interfere with catecholamine action and cause hypotension unresponsive to inotropics.

Metabolic acidosis is a sign of underlying lack of adequate oxygen delivery or consumption and should be treated with more aggressive resuscitation, not exogenous bicarbonate

Life-threatening acidemia (pH <7.2) initially may be buffered by the administration of sodium bicarbonate to improve the pH. However, be aware that no survival benefit to this practice has been documented.

Coagulation studies generally produce normal results in the majority of patients with severe hemorrhage early in the course.

The notable exceptions are patients who are on warfarin, low molecular weight heparin, or antiplatelet medications or those patients with severe preexisting hepatic insufficiency.

• Qualitative platelet dysfunction can be inferred in those patients with a clinical coagulopathy and normal PT and aPTT values. Obviously, abnormal PT or aPTT values should be corrected emergently in the context of severe hemorrhage.

Electrolyte studies usually are not helpful in the acute setting. After massive resuscitation, certain abnormalities can occur.

• Sodium and chloride may increase significantly with administration of large amounts of isotonic sodium chloride. Hyperchloremia may cause a non–ion gap acidosis and significantly worsen an existing acidosis.

Calcium levels may fall with large-volume, rapid blood transfusions. This is secondary to chelation of the calcium by the ethylenediaminetetraacetic acid (EDTA) preservative in stored blood.

potassium levels may rise with large-volume blood transfusions.

Creatinine and blood urea nitrogen usually are within normal limits unless preexisting renal disease is present.

A blood specimen for type and crossmatch should be obtained as soon as the patient arrives.

For patients who are actively bleeding, 4 U of packed red blood cells (PRBCs) should be prepared, along with 4 U of fresh frozen plasma (FFP).

Platelets may be obtained as well, depending on the physician's estimation of the likelihood of the need for platelet transfusion (less commonly needed compared to FFP).

Imaging studies are aimed at identifying the source of bleeding.

In many types of severe hemorrhage, therapeutic interventions, such as exploratory laparotomy, will preclude comprehensive diagnostic studies.

Imaging Studies

◦ Chest radiographs indicate a diagnosis of hemothorax by showing a large opacity in one or both lung fields.

◦ Hemothoraces large enough to cause shock

usually are obvious as a complete whiteout of one pleural space.

Chest radiographs

◦ Abdominal radiographs are rarely helpful. ◦ Occasionally, a radiograph will have a diffuse ground

glass appearance, suggesting a large amount of intraperitoneal fluid, but this sign is not reliable.

◦ Rarely, a ruptured abdominal aortic aneurysm can be diagnosed by noting an incomplete shell (calcified wall) of a dilated aorta.

• Loss of the psoas shadow unilaterally also can suggest retroperitoneal blood.

Abdominal radiographs

(CT) scan is sensitive and specific for diagnosing intrathoracic, intra-abdominal, and retroperitoneal bleeding. It is the test of choice for diagnosing bleeding in these cavities.

• CT scan only has an adjunctive role in the diagnosis of GI bleeding when other tests have suggested a mass lesion as part of the disease process.

Computed tomography scan

• Ultrasound is rapidly replacing CT scan as the diagnostic test of choice for the identification of hemorrhage in major body cavities.

• It is, of course, limited in its ability to evaluate the retroperitoneum.

• Retroperitoneal evaluation remains the purview of the CT scan.

Ultrasound

(FAST) examination realistically has replaced diagnostic peritoneal lavage as the test of choice for identifying intraperitoneal fluid in the trauma patient.

• The FAST examination includes 4 anatomical views of the pericardium, abdomen, and pelvis that attempt to identify free intra-abdominal fluid.

Angiography is extremely useful in the diagnosis of acute hemorrhage from many different sources. Its utility is limited by the availability of an angiographer on a timely basis.

In cases of lower GI bleeding, angiography is one of the best tests to localize a bleeding source. Angiography usually can detect bleeding that is at least 1-2 mL/min.

• Angiography can be used for diagnosis and management of severe bleeding from pelvic fractures. Although most bleeding from severe pelvic fractures is venous in origin, occasional significant arterial bleeding can be diagnosed and treated effectively with embolization.

Severe liver injuries pose a challenge to the trauma surgeon because of the large amounts of blood loss and the difficulty in gaining surgical control quickly.

Many severe liver injuries now are being diagnosed and treated with angiographic embolization.

Angiography is increasingly considered first-line intervention (before laparotomy) for severe liver injuries in centers that are equipped to perform rapid angiography and angiographic intervention.

Similar methods may be used for other solid organ injuries, such as the spleen and kidney.

• The role of angiography in upper GI bleeding is more limited and Hemobilia is a rare cause of upper GI bleeding.

• If blood definitely is observed emanating from the ampulla of Vater, angiography should be performed to localize and control the source of bleeding.

◦ A tagged red blood cell scan may help differentiate upper from lower GI bleeding and may provide anatomic information, such as identifying bleeding from the right versus left colon.

◦ Overlap of structures will confound the utility and accuracy of this test.

◦ The test requires a significant amount of time to complete, but it is very sensitive, detecting bleeding as slow as 0.5 mL/min.

Nuclear medicine scanning can be used to localize GI bleeding:

Diagnostic peritoneal lavage is a bedside procedure that utilizes a small midline laparotomy and insertion of a catheter directly into the peritoneal cavity.

• The intent of diagnostic peritoneal lavage is to determine if significant intra-abdominal bleeding or injuries to hollow organs are present.

Procedures:

• If more than 5 mL of blood is aspirated, the test result is said to be grossly positive and laparotomy usually is indicated.

Central venous access is considered an adjunct to large-bore (16- or 14-gauge) peripheral IV lines.

Large-bore (12F) central resuscitation lines are used for volume resuscitation .

• If significant intra-abdominal bleeding from a venous injury is suspected, volume lines should be avoided in the femoral veins.

Chest tube:

-The initial management of a hemothorax involves the insertion of a large-caliber chest tube for drainage, or open thoracotomy.

-In most patients with a hemothorax, tube thoracostomy alone is sufficient.

-Surgical exploration with open thoracotomy is mandated in the presence of persistent bleeding; the presence of more than 1500 mL of blood in the initial chest tube drainage; or drainage of more than 200 mL/h for 2-4 hours.

Medical Care:

-The primary treatment of hemorrhagic shock is to control the source of bleeding as soon as possible and to replace fluid.

-In controlled hemorrhagic shock (CHS), where the source of bleeding has been occluded, fluid replacement is aimed toward normalization of hemodynamic parameters.

Treatment

In(UCHS), in which the bleeding has temporarily stopped because of hypotension, vasoconstriction, and clot formation, fluid treatment is aimed at restoration of radial pulse or restoration of sensorium or obtaining a blood pressure of 80 mm Hg by aliquots of 250 mL of lactated Ringer's solution (hypotensive resuscitation).

When evacuation time is shorter than 1 hour (usually urban trauma), immediate evacuation to a surgical facility is indicated after airway and breathing (A, B) have been secured ("scoop and run").

( Precious time is not wasted by introducing an intravenous line.)

When expected evacuation time exceeds 1 hour, an intravenous line is introduced and fluid treatment is started before evacuation.

Crystalloid is the first fluid of choice for resuscitation. Immediately administer 2 L of isotonic sodium chloride solution or lactated Ringer’s solution in response to shock from blood loss.

Fluid administration should continue until the patient's hemodynamics become stabilized.

Because crystalloids quickly leak from the vascular space, each liter of fluid expands the blood volume by 20-30%; therefore, 3 L of fluid need to be administered to raise the intravascular volume by 1 L.

colloids restore volume in a 1:1 ratio. Currently available colloids include human albumin, hydroxy-ethyl starch products (mixed in either 0.9% isotonic sodium chloride solution or lactated Ringer’s solution), or hypertonic saline-dextran combinations.

The sole product that is avoided routinely in large-volume (>1500 mL/d) restoration is the hydroxy-ethyl starch product mixed in 0.9% isotonic sodium chloride solution because it has been associated with the induction of coagulopathy.

PRBCs should be transfused if the patient remains unstable after 2000 mL of crystalloid resuscitation.

For acute situations, O-negative noncrossmatched blood should be administered.

Administer 2 U rapidly, and note the response.

If at all possible, blood and crystalloid infusions should be delivered through a fluid warmer.

A blood sample for type and cross should be drawn, preferably before blood transfusions are begun.

Start type-specific blood when available.

Patients who require large amounts of transfusion inevitably will become coagulopathic.

FFP generally is infused when the patient shows signs of coagulopathy, usually after 6-8 U of PRBCs.

Platelets become depleted with large blood transfusions so Platelet transfusion is also recommended when a coagulopathy develops.

Acute life-threatening bleeding within the abdominal or thoracic cavity is an indication for operation.

Retroperitoneal bleeding is difficult to

control operatively and generally is treated nonoperatively.

Surgical Care:

Severe upper GI bleeds should be managed first by EGD, with the possibility of cauterizing or injecting the bleeding source with epinephrine.

Failure of endoscopic management usually is an indication for surgery.

Confirm the location of a lower GI bleed before operative intervention is performed.

On occasion, consultation with a hematologist is essential.

This is especially true if the coagulopathy fails to be corrected with standard measures.

Increasingly recognized are the entities of heparin-induced thrombocytopenia and acquired antibodies to native clotting factors.

Consultations

These may include IV gamma-globulin infusion, plasmapheresis, or, simply, large-volume clotting factor repletion.

Patients with hemorrhagic shock are at risk for acute tubular necrosis, acute lung injury, transfusion-related acute lung injury, infections (principally nosocomial and related to operative sites or indwelling catheters), and multiple organ dysfunction syndrome, with its attendant risk of death

Further Inpatient Care

with hemorrhagic shock are often unable to mount an appropriate bone marrow response in the acute setting with regard to red blood cell production.

Using erythropoietin (40,000 U/wk) in combination with supplemental iron and vitamin C to boost production is useful.

The primary complication is death.

The entire spectrum of organ failures may be the sequelae of resuscitated hemorrhagic shock.

The cascade of systemic inflammatory response syndrome (SIRS) progressing to multiple organ failure syndrome complicates the cases of approximately 30-70% of patients who present with hemorrhagic shock and survive their initial resuscitation.

Complications

Prognosis is related to the ability to be resuscitated from shock, as well as the underlying illness or injury, not the presentation of hemorrhagic shock.

Prognosis

Implies the hemodynamic instability due to host inflammatory response to the infection

There are local and systemic responses to infection and

these responses could be hypo or hyperdynamic

Septic shock:

May result from infection with gram –ve or +ve bacteria ,viruse ,protozoa

The gram +ve –massive fluid losses secondary to dissemination of potent exotoxin with out bactermia

Causative organism include clostridium ,staph and strept.

Characterized by hypotension with normal UOP and unaltered mental status.

Prognosis is good with the treatment.

Treatment –appropriate antibiotic, surgical drainage or debridement if necessary and IV fluid.

The gram –ve_ initiated by endotoxins in the cell wall of gram negative.

Causative organism –GI flora including coli forms and anaerobic bacilli e.g., klebsiella , enterobacteriaceae , serratia and bacteroides.

Common source urinary tract, pulmonary ,GI, burns

Early identification of source of infection and appropriate antibiotic

Foley cath to moniter the UOP. IV fluid Vasopressors ,in tropes. Support individual organ system. New therapies directed at specific.

inflammatory mediators of sepsis include antibodies.

Treatment:

Fungal-causative organism are commonly Candida

Seen in neutropenic ,immunosuppressed, multitauma or burn Pt.

Risk factor parenteral nutrition, invasive monitors, and broad spectrum antibiotics

When its reach the intravascular compartment widespread dissemination can occur.

Can cause micro abscesses.

Characterized by high fever and rigors

Blood culture –ve in 50%

Treatment _antifungal

“Our greatest glory is not in never falling,but in rising every time we

fall”

Thank you

Dr. amani alhaddad