The best evidence exists for the treatment of septic shock in adults and as the pathophysiology appears similar in children and other types of shock treatment this has been extrapolated to these areas. Management may include securing the airway via intubation if necessary to decrease the work of breathing and for guarding against respiratory arrest. Oxygen supplementation, intravenous fluids, passive leg raising (not Trendelenburg position) should be started and blood transfusions added if blood loss is severe. It is important to keep the person warm as well as adequately manage pain and anxiety as these can increase oxygen consumption.

Because lowered blood pressure in septic shock contributes to poor perfusion, fluid resuscitation is an initial treatment to increase blood volume. Crystalloids such as normal saline and lactated Ringer's solution are recommended as the initial fluid of choice, while the use of colloid solutions such as hydroxyethyl starch have not shown any advantage or decrease in mortality. When large quantities of fluids are given, administering albumin has shown some benefit.

Aggressive intravenous fluids are recommended in most types of shock (e.g. 1–2 liter normal saline bolus over 10 minutes or 20 ml/kg in a child) which is usually instituted as the person is being further evaluated. Which intravenous fluid is superior, colloids or crystalloids, remains undetermined. Thus as crystalloids are less expensive they are recommended. If the person remains in shock after initial resuscitation packed red blood cells should be administered to keep the hemoglobin greater than 100 g/l.

For those with haemorrhagic shock the current evidence supports limiting the use of fluids for penetrating thorax and abdominal injuries allowing mild hypotension to persist (known as permissive hypotension). Targets include a mean arterial pressure of 60 mmHg, a systolic blood pressure of 70–90 mmHg, or until their adequate mentation and peripheral pulses.

Treatment primarily consists of the following:

1. Giving intravenous fluids

2. Early antibiotic administration

3. Early goal directed therapy

4. Rapid source identification and control

5. Support of major organ dysfunction

6. High fever

The choice of fluids for resuscitation remains an area of research, the Surviving Sepsis Campaign an international consortium of experts, did not find adequate evidence to support the superiority crystalloid fluids versus colloid fluids. Drugs such as, pyridoxalated hemoglobin polyoxyethylene, which scavenge nitric oxide from the blood have been investigated. As well as methylene blue which may inhibit the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway which has been suggested to play a significant role in distributive shock.

The main goals of treatment in distributive shock are to reverse the underlying cause and achieve hemodynamic stabilization. Immediate treatment involves fluid resuscitation and the use of vasoactive drugs, both vasopressors and inotropes. Hydrocortisone is used for patients whose hypotension does not respond to fluid resuscitation and vasopressors. Opening and keeping open the microcirculation is a consideration in the treatment of distributive shock, as a result limiting the use of vasopressors has been suggested. Control of inflammation, vascular function and coagulation to correct pathological differences in blood flow and microvascular shunting has been pointed to as a potentially important adjunct goal in the treatment of distributive shock.

Patients with septic shock are treated with antimicrobial drugs to treat the causative infection. Some sources of infection require surgical intervention including necrotizing fasciitis, cholangitis, abscess, intestinal ischemia, or infected medical devices.

Anaphylactic shock is treated with epinephrine.

Neurogenic shock is a distributive type of shock resulting in low blood pressure, occasionally with a slowed heart rate, that is attributed to the disruption of the autonomic pathways within the spinal cord. It can occur after damage to the central nervous system such as spinal cord injury. Low blood pressure occurs due to decreased systemic vascular resistance resulting in pooling of blood within the extremities lacking sympathetic tone. The slowed heart rate results from unopposed vagal activity and has been found to be exacerbated by hypoxia and endobronchial suction.

Neurogenic shock can be a potentially devastating complication, leading to organ dysfunction and death if not promptly recognized and treated. It is not to be confused with spinal shock, which is not circulatory in nature.

Emergency oxygen should be immediately employed to increase the efficiency of the patient's remaining blood supply. This intervention can be life-saving.

The use of intravenous fluids (IVs) may help compensate for lost fluid volume, but IV fluids cannot carry oxygen in the way that blood can; however, blood substitutes are being developed which can. Infusion of colloid or crystalloid IV fluids will also dilute clotting factors within the blood, increasing the risk of bleeding. It is current best practice to allow permissive hypotension in patients suffering from hypovolemic shock, both to ensure clotting factors are not overly diluted and also to stop blood pressure being artificially raised to a point where it "blows off" clots that have formed.

Hypovolemia is a state of decreased blood volume; more specifically, decrease in volume of blood plasma. It is thus the intravascular component of volume contraction (or loss of blood volume due to things such as bleeding or dehydration), but, as it also is the most essential one, "hypovolemia" and volume contraction are sometimes used synonymously.

Hypovolemia is characterized by sodium depletion (salt depletion) and thus differs from dehydration, which is defined as excessive loss of body water.

The second stage features the reabsorption of the initially extravasated fluid and albumin from the tissues, and it usually lasts 1 to 2 days. Intravascular fluid overload leads to polyuria and can cause flash pulmonary edema and cardiac arrest, with possibly fatal consequences. Death from SCLS typically occurs during this recruitment phase because of pulmonary edema arising from excessive intravenous fluid administration during the earlier leak phase. The severity of the problem depends on to the quantity of fluid supplied in the initial phase, the damage that may have been sustained by the kidneys, and the promptness with which diuretics are administered to help the patient discharge the accumulated fluids quickly. A recent study of 59 acute episodes occurring in 37 hospitalized SCLS patients concluded that high-volume fluid therapy was independently associated with poorer clinical outcomes, and that the main complications of SCLS episodes were recovery-phase pulmonary edema (24%), cardiac arrhythmia (24%), compartment syndrome (20%), and acquired infections (19%).

The prevention of episodes of SCLS has involved two approaches. The first has long been identified with the Mayo Clinic, and it recommended treatment with beta agonists such as terbutaline, phosphodiesterase-inhibitor theophylline, and leukotriene-receptor antagonists montelukast sodium.

The rationale for use of these drugs was their ability to increase intracellular cyclic AMP (adenosine monophosphate) levels, which might counteract inflammatory signaling pathways that induce endothelial permeability. It was the standard of care until the early 2000s, but was sidelined afterwards because patients frequently experienced renewed episodes of SCLS, and because these drugs were poorly tolerated due to their unpleasant side effects.

The second, more recent approach pioneered in France during the last decade (early 2000s) involves monthly intravenous infusions of immunoglobulins (IVIG), with an initial dose of 2 gr/kg/month of body weight, which has proven very successful as per abundant case-report evidence from around the world.

IVIG has long been used for the treatment of autoimmune and MGUS-associated syndromes, because of its potential immunomodulatory and anticytokine properties. The precise mechanism of action of IVIG in patients with SCLS is unknown, but it is likely that it neutralizes their proinflammatory cytokines that provoke endothelial dysfunction. A recent review of clinical experience with 69 mostly European SCLS patients found that preventive treatment with IVIG was the strongest factor associated with their survival, such that an IVIG therapy should be the first-line preventive agent for SCLS patients. According to a recent NIH survey of patient experience, IVIG prophylaxis is associated with a dramatic reduction in the occurrence of SCLS episodes in most patients, with minimal side effects, such that it may be considered as frontline therapy for those with a clear-cut diagnosis of SCLS and a history of recurrent episodes.

In mostly European experience with 69 patients during 1996-2016, the 5- and 10-year survival rates for SCLS patients were 78% and 69%, respectively, but the survivors received significantly more frequent preventive treatment with IVIG than did non-survivors. Five- and 10-year survival rates in patients treated with IVIG were 91% and 77%, respectively, compared to 47% and 37% in patients not treated with IVIG. Moreover, better identification and management of this condition appears to be resulting in lower mortality and improving survival and quality-of-life results as of late.

A circulatory collapse is defined as a general or specific failure of the circulation, either cardiac or peripheral in nature.

Although the mechanisms, causes and clinical syndromes are different the pathogenesis is the same, the circulatory system fails to maintain the supply of oxygen and other nutrients to the tissues and to remove the carbon dioxide and other metabolites from them. The failure may be hypovolemic, distributive.

A common cause of this could be shock or trauma from injury or surgery.

Neurogenic shock can result from severe central nervous system damage (brain injury, cervical or high thoracic spinal cord). In more simple terms: the trauma causes a sudden loss of background sympathetic stimulation to the blood vessels. This causes them to relax (vasodilation) resulting in a sudden decrease in blood pressure (secondary to a decrease in peripheral vascular resistance).

Neurogenic shock results from damage to the spinal cord above the level of the 6th thoracic vertebra. It is found in about half of people who suffer spinal cord injury within the first 24 hours, and usually doesn't go away for one to three weeks.

Surgical shock is the shock to the circulation resulting from surgery. It is commonly due to a loss of blood which results in insufficient blood volume.

Electrical injury is a physiological reaction caused by electric current passing through the (human) body. Electric shock occurs upon contact of a (human) body part with any source of electricity that causes a sufficient magnitude of current to pass through the victim's flesh, viscera or hair. Physical contact with energized wiring or devices is the most common cause of an electric shock. In cases of exposure to high voltages, such as on a power transmission tower, physical contact with energized wiring or objects may not be necessary to cause electric shock, as the voltage may be sufficient to "jump" the air gap between the electrical device and the victim.

The injury related to electric shock depends on the magnitude of the current. Very small currents may be imperceptible or produce a light tingling sensation. A shock caused by low current that would normally be harmless could startle an individual and cause injury due to suddenly jerking away from the source of electricity, resulting in one striking a stationary object, dropping an object being held or falling. Stronger currents may cause some degree of discomfort or pain, while more intense currents may induce involuntary muscle contractions, preventing the victim from breaking free of the source of electricity. Still larger currents usually result in tissue damage and may trigger fibrillation of the heart or cardiac arrest, any of which may ultimately be fatal. If death results from an electric shock the cause of death is generally referred to as electrocution.

Fulminant infection from meningococci bacteria in the bloodstream is a medical emergency and requires emergent treatment with adequate antibiotics. Benzylpenicillin was once the drug of choice with chloramphenicol as a good alternative in allergic patients. Ceftriaxone is an antibiotic commonly employed today. Hydrocortisone can sometimes reverse the adrenal insufficiency. Plastic surgery and tissue grafting are sometimes needed to treat tissue necrosis resulting from the infection.

Heating due to resistance can cause extensive and deep burns. Voltage levels of 500 to 1000 volts tend to cause internal burns due to the large energy (which is proportional to the duration multiplied by the square of the voltage divided by resistance) available from the source. Damage due to current is through tissue heating. For most cases of high-energy electrical trauma, the Joule heating in the deeper tissues along the extremity will reach damaging temperatures in a few seconds.

A "general failure" is one that occurs across a wide range of locations in the body, such as systemic shock after the loss of a large amount of blood collapsing all the circulatory systems in the legs. A "specific failure" can be traced to a particular point, such as a clot.

Cardiac circulatory collapse affects the vessels of the heart such as the aorta and is almost always fatal. It is sometimes referred to as "acute" circulatory failure.

Peripheral circulatory collapse involves outlying arteries and veins in the body and can result in gangrene, organ failure or other serious complications. This form is sometimes called "peripheral vascular failure", "shock" or "peripheral vascular shutdown".

A milder or preliminary form of circulatory collapse is circulatory insufficiency.

The VHF viruses are spread in a variety of ways. Some may be transmitted to humans through a respiratory route. According to Soviet defector Ken Alibek, Soviet scientists concluded China may have tried to weaponise a VHF virus during the late 1980's but discontinued to do so after an outbreak . The virus is considered by military medical planners to have a potential for aerosol dissemination, weaponizaton, or likelihood for confusion with similar agents that might be weaponized.

Hematemesis is treated as a medical emergency. The most vital distinction is whether there is blood loss sufficient to cause shock.

Rodent control in and around the home remains the primary prevention strategy, as well as eliminating contact with rodents in the workplace and campsite. Closed storage sheds and cabins are often ideal sites for rodent infestations. Airing out of such spaces prior to use is recommended. Avoid direct contact with rodent droppings and wear a mask to avoid inhalation of aerosolized rodent secretions.

With the exception of yellow fever vaccine neither vaccines nor experimental vaccines are readily available. Prophylactic (preventive) ribavirin may be effective for some bunyavirus and arenavirus infections (again, available only as IND).

VHF isolation guidelines dictate that all VHF patients (with the exception of dengue patients) should be cared for using strict contact precautions, including hand hygiene, double gloves, gowns, shoe and leg coverings, and faceshield or goggles. Lassa, CCHF, Ebola, and Marburg viruses may be particularly prone to nosocomial (hospital-based) spread. Airborne precautions should be utilized including, at a minimum, a fit-tested, HEPA filter-equipped respirator (such as an N-95 mask), a battery-powered, air-purifying respirator, or a positive pressure supplied air respirator to be worn by personnel coming within 1,8 meter (six feet) of a VHF patient. Multiple patients should be cohorted (sequestered) to a separate building or a ward with an isolated air-handling system. Environmental decontamination is typically accomplished with hypochlorite (e.g. bleach) or phenolic disinfectants.

Investigational vaccines exist for Argentine hemorrhagic fever and RVF; however, neither is approved by FDA or commonly available in the United States.

The structure of the attachment glycoprotein has been determined by X-ray crystallography and this glycoprotein is likely to be an essential component of any successful vaccine.

If this is not the case, the patient is generally administered a proton pump inhibitor (e.g. omeprazole), given blood transfusions (if the level of hemoglobin is extremely low, that is less than 8.0 g/dL or 4.5–5.0 mmol/L), and kept NPO, which stands for "nil per os" (Latin for "nothing by mouth", or no eating or drinking) until endoscopy can be arranged. Adequate venous access (large-bore cannulas or a central venous catheter) is generally obtained in case the patient suffers a further bleed and becomes unstable.

Intracerebral hemorrhages is a severe condition requiring prompt medical attention. Treatment goals include lifesaving interventions, supportive measures, and control of symptoms. Treatment depends on the location, extent, and cause of the bleeding. Often, treatment can reverse the damage that has been done.

A craniotomy is sometimes done to remove blood, abnormal blood vessels, or a tumor. Medications may be used to reduce swelling, prevent seizures, lower blood pressure, and control pain.