Septic shock is a syndrome marked by altered hemodynamics decreased tissue perfusion and loss of cellular energy. It develops primarily because of the body's immune and inflammatory responses to the endotoxins released when the cell wall of gram-negative bacteria is destroyed (see illustration).
The gram-negative bacteria that usually cause septic shock are all normal, symbiotic residents of the gastrointestinal tract. Escherichia coli is most often to blame (40% of cases), followed by Klebsiella-Enterobacteriaceae-Serratia (20%) and Pseudomonas aeruginosa (also 20%), and Bacteroides and Proteus (both 10%).
Patients at risk
Before we heap too much blame on these offending organisms, remember that it takes a vulnerable host as well as an aggressive guest to cause disease. The patients at greatest risk for septic shock are those whose health has already been compromised in some way (see chart Who's at Risk for Septic Shock).
Even in a hospital with a top-notch housekeeping department, gram-negative organisms abound mostly in feces. These pathogens most often spread through poor hand washing.
Airborne transmission also occurs-many malnourished debilitated patients have gram-negative respiratory infections such as Pseudomonas and Klebsiella. Studies have shown that within 48 hours after a patient is admitted to a hospital the flora in his oropharynx changes to predominantly gram-negative. In many cases respiratory treatments such as incentive spirometry push these flora into vulnerable lung tissue.
In the case of Mr. DeCristo, the spontaneous rupture of his gangrenous gallbladder dumped lethal gram-negative bacteria, mostly E. coli into his peritoneal cavity. This triggered a general inflammatory reaction, which made the blood vessels in the area more permeable, allowing the bacteria to enter the blood. The infection rapidly became systemic.
As soon as the bacteria entered his blood, Mr. DeCristo's reticuloendothelial and complement systems began to destroy the invading organisms. Unfortunately, the destruction of gram-negative bacteria releases large amounts of a lipopolysaccharide called lipid A. This endotoxin initiates a massive self-perpetuating immune system response which if unchecked will prove fatal.
Warm shock-the first phase
Septic shock can be broken down into two different types of shock: warm (or hyperdynamic) shock and cold (or hypodynamic) shock.
Warm shock characterized by high cardiac output and low peripheral vascular resistance occurs first. Vasodilation from the effects of histamine, bradykinins, serotonin, and endorphins dramatically decrease total peripheral vascular resistance. It also makes capillaries more permeable causing leakage and fluid shifting into tissues and physiologic third spaces.
Two other factors contribute to vascular fluid loss-fever (caused by endogenous pyrogen released by leukocytes attacking gram-negative bacteria) and the patient's high respiratory rate Mr. DeCristo's postoperative temperature, you'll 102.5�F and his respiratory rate was 32.
Another sign to look for is profound diuresis. This develops because of the high osmotic load being handled by the kidneys, the result of all those dead and dying bacteria, phagocytie cells, tissue breakdown, and end products of cellular metabolism.
To compensate for the patient's profoundly diminished plasma volume, catecholamines increase cardiac output and myocardial contractility. But these effects won't be strong enough to keep his blood pressure up. Eventually, tissue perfusion becomes inadequate resulting in loss of cellular energy and increased lactic acid production.
Unusually rapid respirations
Let's go back for a minute to Mr. DeCristo's rapid respiration-a very�
The patient in warm shock will have an unusually high respiratory rate. He'll undoubtedly have a fever and may be in the early stages of metabolic acidosis, but neither of these signs will be severe enough to explain his rapid respirations. Many authorities believe the rapid respiration result from the effect of the bacterial endotoxins on the medullary respiratory center.
Whatever its cause, the high respiratory rate can cause a profound respiratory alkalosis that counterbalances lactic acidemia It may actually shift the patient's pH toward alkalosis.
What about arterial blood gas(ABG)analysis? What will that show? Probably two things-both metabolic acidosis and respiratory rate may keep his PaO2 elevated in this early stage of septic shock. And because he won't be using up that muck oxygen saturation of mixed venous blood will most likely of mixed venous blood will most likely be greater than the normal 80%.
Clotting factors used up
Something else is going on, too-excessive activation of the clotting mechanism, resulting in coagulopathy. The complement system contributes to the damage of the vascular endothelium and to neutrophil aggregation, while the Hageman factor accelerates clotting and causes multiple fibrin clots to form.
These clots plug up small capillaries, producing petechiae and altered blood flow, which appears as "creeping" mottling of the legs. The mottling starts in the feet and works its way up to the knees. You'll recall that this sign was noted by Mr. DeCristo's nurse. As clotting factors are used up in the microcirculation serum levels of clotting Factors V, VIII, and XIII, as well as platelet and fibrinogen counts will be below normal.
Meanwhile decreased cerebral perfusion may produce signs of impaired mental status-vague delayed responses for example with restlessness and confusion. Some authorities consider this a characteristic early sign of septic shock. Others aren't so sure they point out that many patients are alert and oriented until multisystem failure sets in. The release of endorphins, the body's natural opiates may be responsible for keeping the patient relatively comfortable making it that muck more difficult to recognize the trouble he's going into.
Cold shock-ominous late stage
Most patient swill remain in warm shock for 6 to 72 hours before entering cold shock (also known as low-output or high-resistance shock). This late and nearly irreversible phase of septic shock is usually indistinguishable from terminal hypovolemic shock.
Two ominous signs of could shock are a subnormal temperature and a low white blood cell count (with many immature cells). By the time the patient gets to this stage, his hypotension and hypoperfusion are profound. His skin will be cold and mottled in a more generalized fashion-not just below the knees, as in warm shock. Pulse and respirations will still be rapid because of the continued firing of sympathetic nerves and increased catecholamine levels.
Cardiac output, however, decreases during cold shock. The catecholamines casue selective vasoconstriction of the renal, pulmonary, and splanchnic circulations. This effect coupled with conagulopathy in the microcirculations releases myocardial depressant factor from pancreatic cells. More beta endotoxins�block pain impulses but further depresses the myocardium.
Eventually, cold shock brings multisystem failure-pulmonary edema, adult respiratory distress syndrome, liver and kidney failure, even hemorrhaging from disseminated intravascular coagulation. The patient's mental status and reflexes deteriorate because of hypoperfusion and cerebral microemboli. His ABGs will show uncompensated hypoxemia, acidemia, and hypoventilation with shunting.
Early warning signs
The lesson here is clear: Try to detect septic shock as early as possible. You don't want you rpatient to get into the cold shock phase. The chart Contrasting Warm and Cold Septic Shock will help you distinguish between the two phases.
The more familiar you are with the clinical pattern of warm shock, the better your chances of detecting septic shock before it's too late. The following clues should alert you to the possibility that your patient is entering the warm phase of septic shock.
- He falls into one of the high risk.
- He has an infection, especially on that's known to be gram-negative
- His blood pressure has fallen 25% below what's normal for him.
- He's hyperventilating but
doesn't have any respiratory dysfunction or acidosis.
- He has a high fever with hot, dry, flushed skin.
- his legs feel cool and look mottled.
If you detect these early warning signs in a patient, get in touch with his doctor immediately. Draw blood and send it to the laboratory for stat analysis. You'll need a complete blood count. ABG analysis, liver function tests, culture and sensitivity testing, and a type and crossmatch. A urine sample should also be obtained and analyzed.
The patient's vital signs and neurologic status, especially level of consciousness, must be assessed frequently - every 15 minutes. Inspect his skin closely for color, mottling, and impending breakdown.
Treating septic shock
If you have a patient in septic shock, you can expect his therapy to be geared toward these three goals : (1) finding and eradicating the cause of the gram-negative infection; (2) supporting the cardiovascular system; and (3) preventing or treating complications.
The cause of the gram-negative infection will be removed if possible. In Mr. DeCristo's case, his infected gallbladder normally wouldn't have been removed until the infection had abated somewhat. But his surgeons had to wigh that risk against the greater risk of a spintaneous rupture before surgery. As it turned out, even though bacteria spilled into Mr. DeCristo's peritoneum, immediate flushing of the area with antibiotic solution helped minimize the consequences.
Because of the severe loss of vascular fluid and its sequestration in tissues, the patient may need up to 10 liters of fluid just to keep him from getting any worse. Fluids must be given cautiously, in increments, because of the ever present risk of myocardial depression and heart failure.
You'll be responsible for monitoring your patient's pulmonary artery pressure carefully. A flow-directed pulmonary artery catheter will be inserted. Invasive procedurea are usually constraindicated in septic shock, but monitoring treatment without a pulmonary artery catheter is difficult.
Administering fluids
The fluids of choice are colloids (plasma volume expanders) and crystalloids (balanced salt solutions). Fresh frozen plasma may help restore clotting factors to prevent disseminated intravascular coagulation.
You'll need to insert large-bore I.V. cannulas for the rapid administration of fluids, medication, and blood products. A flow chart with lab values, intakes and output measurements, and vital signs will help you monitor the patient's status.
Watch for signs of dehydration such as decreased eyeball tension, dry mucous membranes, and longitudinal furrows in the tongue. Keep in mind, though, that because of fluid sequestration, you may not see any signs of dehydration other than hypertension.
Of course, once fluid resuscitation begins, you'll also need to watch for signs of overhydration, such as dependent edema and basilar crackles in the lungs. Weighing the patient (on a bed scale) can provide valuable information about his overall hydration status. Remember that a gain of only 1 or 2 pounds (0.5 to 1 kg) can indicate sequestration of 1 liter of fluid.
Cautious use of antibiotics
You can expect to administer antibiotics - typically, a combination of drugs such as a cephalosporin, an aminoglycoside, and a penicillin derivative (usually ampicillin). As with fluids, these drugs must be given cautiously. Usually, the patient's cardiovascular system will be stablized first. Otherwise, antibiotics will just hasten bacterial destruction and cause more endotoxins to be released, exacerbating the patient's condition.
Until the fluids and antibiotics take effect, you'll need to control the patient's temperature to prevent central nervous system damage. If his fever is above 102�F (38.9�C), use acetaminophen suppositories, cool sponges, and a hypothermia blankets, if necessary, to bring it down. Two precautions here : Protect the patient's skin from "frostbite" by rubbing it with lotion and covering mottled areas. Watch for a sudden drop in temperature that may herald the onset of cold shock.
Vasopressssors and inotropic agents
For the patient in warm shock, fluid resuscitation and antibiotics should be enough to pull him out of it. However, if he's gone into cold shock for if he's still in warm shock but debilitated, he'll need supplemental drug therapy.
Vasopressors and inotropic agents may be given if fluids fail to maintain the patient's blood pressure at the desired level. Dopamine, in low doses, is the drug of choice because it stimulates vascular dopaminergic receptors that dilate splanchnic, mesenteric, and renal vessels. It also increases cardiac contractility.
Nitroprusside or nitroglycerin may be given with dopamine (or dobutamine) during cold shock. Nitroprusside reduces preload and afterload by dilating veins and arteries; when used with dopamine, it increases cardiac output and decreases peripheral vascular resistence.
Nitroglycerin also helps improve cardiac output and decrease peripheral vascular resistance. Alpha-adrenergic drugs, such as norepinphrine, are always contraindicated because they cause vasoconstriction, which would increase peripheral vascular resistance.
Ionized calcium is vital to supporting the cardiovascular system, especially if the patient is receiving transfusions. One or 2 grams of calcium given over a 10 to 30 minute period can improve cardiac output.
The use of digitalis is controversial, particular in patients with kidney problems. If this drug isn't readily excretely, digitalis toxicity may develope precipating dysrhythmias. Diuretics must be used with caution because they may further deplete intrvascular volume and exacerabate dehydration.
Steroids - yes or no?
Another controversial aspect of treatment involves corticosteroids. Some researchers feel that the judicious use of steroids is justified. They point to the fact that 15% of septic shock patients have adrenal insufficiency, a significant predisposing factor.
Also, steroids produce several effects that can help combat the pathologic processes at work in septic shock. For example, they stablize the capillary and lysosomal membranes, while curtailing the release of myocardial depressant factor and improving reticuloendothelial function. Steroids also prevent complement activation, leukocytes aggregation, and coagulopathy. And thsy increase cardiovascular function, cellular metabolism, and tissue oxygenation. Although steroid therapy may produce serious adverse reactions, that risk seems to be outweighted by the potential benefits.
Other adjunctive treaments have proven effective to some degree. For example, any one of the following drugs might be administered during warm shock:
One experimental treatment involves an antiendotoxin serum, a hyperimmune human serum obtained by injecting a mutant strain of E. Coli into healty subjects. The antibiotics produced in this way bind with, inactivate, and ingest the endotoxin.
During cold shock, I.V. glucose, insulin, and potassium may be ordered to restore depleted cellular energy by facilitating glucose utilization.
Finally, a word about respiratory care, which is vital to preventing complications of pulmonary edema and adult respiratory distress syndrome. You can expect to administer oxygen at 4 liters/minute. If the patient's pulmonary artery wedge pressure rises to dangerously high levels, intubation and mechanical ventilation may be indicated. Positive end-respiratory pressure can help to push fluid out of the lungs and back into the vascular tree. Incasive respiratory care, however, should be used as a last resort because of the risk of gram-negative septicemia developing at a different site.
Better prepared
With the incidence of septic shock on the rise, the chances are good that you'll be seeing many patient's like Mr. DeCristo in the future. I hope you're now even better prepared to identify your patient's at risk for this condition and to watch them closely for early signs of trouble.
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