Shock: 9 commonly taught types

Easy classification map

SHOCK
├─ Hypovolemic
│  ├─ Hemorrhagic
│  └─ Non-hemorrhagic fluid loss
├─ Cardiogenic
├─ Obstructive
└─ Distributive
   ├─ Septic
   ├─ Anaphylactic
   ├─ Neurogenic
   └─ Endocrine

Key hemodynamic pattern

Exam points

• Anaphylactic, septic, and neurogenic shock are distributive shock.
• Obstructive shock may be viewed as a mechanical form of low-output shock, but is usually listed separately.
• Trauma frequently produces mixed shock, particularly hemorrhagic plus obstructive or neurogenic shock.
• The definitive treatment is always directed at the cause: control bleeding, restore volume when appropriate, reperfuse myocardium, relieve obstruction, give antimicrobials/source control in sepsis, intramuscular epinephrine in anaphylaxis, and treat adrenal or thyroid crisis when present.

1. General principles of shock
   • Definition, oxygen delivery, stages, clinical features, monitoring, and initial resuscitation
2. Hemorrhagic shock
   • Blood-loss classes, causes, physiology, diagnosis, damage-control resuscitation
3. Non-hemorrhagic hypovolemic shock
   • GI, renal, skin, and third-space losses; fluid replacement principles
4. Cardiogenic shock
   • MI, arrhythmia, mechanical/valvular causes, pulmonary edema, hemodynamic support
5. Obstructive shock
   • Tamponade, tension pneumothorax, massive pulmonary embolism, and immediate decompression/reperfusion measures
6. Septic shock
   • Sepsis pathophysiology, recognition, cultures, antibiotics, fluids, vasopressors, source control
7. Anaphylactic shock
   • Clinical criteria, emergency intramuscular epinephrine, airway support, adjuncts, observation
8. Neurogenic shock
   • Relation to spinal cord injury, distinction from spinal shock, bradycardia, fluid and vasopressor treatment
9. Endocrine and traumatic shock
   • Adrenal crisis, myxedema coma, thyroid storm; mixed shock in trauma and trauma priorities

• Low volume: hemorrhagic and non-hemorrhagic hypovolemic shock
• Pump failure: cardiogenic shock
• Mechanical blockage: obstructive shock
• Vasodilation/maldistribution: septic, anaphylactic, neurogenic, and many endocrine forms

Shock: all 9 types in detail

1. Definition and core physiology

Oxygen delivery

• Too little circulating volume
• Failure of the heart as a pump
• Mechanical obstruction to blood flow
• Marked vasodilation and maldistribution of blood flow
• Severe endocrine dysfunction
• A mixed process, especially after trauma

Four physiologic categories

---

Common manifestations of shock

Clinical signs

• Hypotension, often late
• Tachycardia, except in neurogenic shock and some endocrine states
• Tachypnea
• Cold, clammy, mottled skin in low-output shock
• Warm extremities and a wide pulse pressure in early distributive shock
• Altered mental status: anxiety, restlessness, confusion, drowsiness
• Oliguria: urine output usually falls
• Delayed capillary refill
• Weak peripheral pulses
• Raised serum lactate and metabolic acidosis

Stages

Important: Normal blood pressure does not exclude early shock.

---

Initial approach to every shocked patient

A. Airway

• Assess airway patency.
• Protect airway if consciousness is impaired.
• Prepare early intubation if there is airway swelling, severe respiratory failure, or inability to protect the airway.

B. Breathing

• Give oxygen if hypoxemic or in respiratory distress.
• Look immediately for tension pneumothorax, pulmonary edema, anaphylaxis, and pulmonary embolism.
• Avoid unnecessary positive-pressure ventilation in severe preload-dependent shock unless airway/ventilation requires it. It can lower venous return and worsen hypotension.

C. Circulation

• Establish two large-bore IV lines or intraosseous access.
• Monitor ECG, blood pressure, oxygen saturation, temperature, consciousness, and urine output.
• Obtain blood tests: CBC, electrolytes, renal and liver function, glucose, ABG/VBG, lactate, coagulation screen, type and crossmatch where bleeding is possible.
• Obtain ECG, bedside ultrasound, and focused imaging according to clinical suspicion.
• Give fluids, blood, vasopressors, inotropes, or urgent cause-specific treatment depending on shock type.

D. Disability

• Assess GCS/mental state and pupils.
• Check bedside blood glucose.

E. Exposure

• Look for bleeding, rash, hives, infection source, trauma, spinal injury, burns, edema, and surgical scars.

Useful endpoints of resuscitation

• Improving mental status and peripheral perfusion
• Falling lactate trend
• Capillary refill improvement
• Urine output generally at least 0.5 mL/kg/hour in adults
• Appropriate blood pressure and MAP, often a starting target of 65 mmHg, individualized to the patient
• Repeated reassessment for fluid responsiveness rather than giving unlimited fluid

---

1. Hemorrhagic shock

Definition

Causes

External bleeding

• Major trauma
• Limb amputation
• Deep lacerations
• Postoperative bleeding
• Postpartum hemorrhage

Internal bleeding

• Ruptured ectopic pregnancy
• Splenic or liver injury
• Pelvic fracture
• Ruptured abdominal aortic aneurysm
• Hemothorax
• Upper or lower GI bleed
• Retroperitoneal bleeding
• Bleeding from anticoagulant therapy

Pathophysiology

1. Reduced circulating volume
2. Reduced venous return and cardiac preload
3. Reduced stroke volume and cardiac output
4. Sympathetic activation with tachycardia and vasoconstriction
5. Reduced perfusion of skin, kidneys, gut, and brain in advanced shock
6. Anaerobic metabolism, lactate elevation, acidosis, coagulopathy, and hypothermia

Lethal triad in trauma

• Hypothermia
• Acidosis
• Coagulopathy

Features

• History of injury, bleeding, hematemesis, melena, vaginal bleeding, or recent surgery
• Tachycardia
• Cool, pale, sweaty skin
• Delayed capillary refill
• Weak pulse and narrow pulse pressure
• Thirst, anxiety, agitation
• Oliguria
• Hypotension is often a late sign
• Flat neck veins, unless another condition is present

Investigation

• CBC and serial hemoglobin, although initial hemoglobin may not reflect acute blood loss
• Coagulation profile and fibrinogen
• Type and crossmatch
• Lactate and blood gas
• FAST ultrasound in trauma
• CT only if the patient is sufficiently stable
• Search specifically for hidden bleeding in chest, abdomen, pelvis, retroperitoneum, and long bones

Management

Immediate priorities

1. Control the bleeding
   • Direct pressure and pressure dressing
   • Tourniquet for life-threatening limb hemorrhage
   • Pelvic binder for suspected unstable pelvic fracture
   • Endoscopic, surgical, interventional radiology, or obstetric control as appropriate
2. Give blood products early when major bleeding is suspected
   • Activate a massive hemorrhage protocol according to local policy.
   • Use balanced resuscitation with packed red cells, plasma, and platelets when indicated.
   • Warm blood products and the patient.
3. Avoid excessive crystalloid
   • Large crystalloid volumes can dilute clotting factors, worsen hypothermia, and increase bleeding.
4. Tranexamic acid
   • In traumatic bleeding, early use within 3 hours may reduce death from bleeding when indicated by local trauma protocol.
   • It is also used in postpartum hemorrhage.
5. Damage-control resuscitation
   • Rapid hemorrhage control
   • Blood component resuscitation
   • Correction of hypothermia, acidosis, hypocalcemia, and coagulopathy
   • Permissive hypotension may be used temporarily in selected penetrating trauma without traumatic brain injury, while definitive bleeding control is being achieved.

Do not delay

---

2. Non-hemorrhagic hypovolemic shock

Definition

Causes

• Severe vomiting or diarrhea
• Poor oral intake and severe dehydration
• Diabetic ketoacidosis or hyperosmolar hyperglycemic state
• Diabetes insipidus
• Osmotic diuresis
• Excess diuretics
• Severe burns with plasma loss
• Pancreatitis
• Bowel obstruction
• Peritonitis
• Nephrotic syndrome
• Third-spacing into bowel, peritoneal cavity, or interstitial tissues

Pathophysiology

• Tachycardia
• Peripheral vasoconstriction
• Activation of the renin-angiotensin-aldosterone system
• Increased antidiuretic hormone secretion

Clinical features

• Dry mouth and tongue
• Reduced skin turgor, though this is unreliable in older adults
• Sunken eyes
• Tachycardia and postural hypotension
• Cool extremities
• Low JVP
• Reduced urine output
• Weight loss
• Features of the underlying cause, such as diarrhea, vomiting, polyuria, burns, abdominal distension, or hyperglycemia

Investigations

• Urea, creatinine, electrolytes
• Blood glucose and ketones when DKA/HHS is possible
• Blood gas and lactate
• Urinalysis
• ECG, especially if potassium disturbance is possible
• Serum osmolality in selected cases
• Ultrasound and abdominal imaging where obstruction, pancreatitis, or third-space loss is suspected

Management

1. Restore intravascular volume
   • Isotonic crystalloid is generally first-line.
   • Use smaller reassessed boluses in elderly patients or those with heart or kidney failure.
2. Correct the specific cause
   • Antiemetics and treatment of diarrhea
   • Insulin and careful electrolyte management for DKA/HHS
   • Desmopressin and free-water management for central diabetes insipidus where appropriate
   • Treatment of burns, pancreatitis, obstruction, or sepsis
3. Correct electrolyte abnormalities
   • Potassium abnormalities are especially dangerous.
   • Do not begin insulin in DKA if severe hypokalemia is present until potassium replacement has started.
4. Monitor response
   • Urine output, blood pressure, capillary refill, mental state, lactate, electrolytes, and glucose.

---

3. Cardiogenic shock

Definition

Causes

Acute coronary syndrome

• Large acute myocardial infarction, especially anterior MI
• Mechanical complications of MI:
  • Ventricular septal rupture
  • Papillary muscle rupture causing acute severe mitral regurgitation
  • Free-wall rupture with tamponade

Other cardiac causes

• Severe acute or chronic heart failure
• Myocarditis
• Stress cardiomyopathy
• Severe tachyarrhythmia or bradyarrhythmia
• Acute severe aortic or mitral regurgitation
• Critical aortic stenosis
• Right ventricular infarction
• Decompensated cardiomyopathy

Pathophysiology

1. Low cardiac output
2. Reduced organ perfusion
3. Compensatory vasoconstriction and increased SVR
4. Raised ventricular filling pressures
5. Pulmonary congestion/edema if left-sided failure predominates
6. Worsening myocardial ischemia from poor coronary perfusion

Features

• Hypotension with tachycardia, though rhythm may be slow in bradyarrhythmia
• Cold, clammy, mottled extremities
• Altered mental status and oliguria
• Chest pain or MI symptoms may be present
• Raised JVP
• Pulmonary crackles, hypoxemia, pulmonary edema
• S3 gallop
• New murmur may suggest acute mitral regurgitation or ventricular septal rupture
• Peripheral edema may occur in pre-existing heart failure

Hemodynamic pattern

• Cardiac output: low
• SVR: high
• PCWP: often high, especially left ventricular failure
• CVP: may be raised, especially in right ventricular failure

Investigations

• ECG and serial troponin
• Echocardiography urgently:
  • LV/RV function
  • Valve failure
  • Mechanical MI complication
  • Pericardial effusion
• Chest radiograph for pulmonary edema
• Bedside ultrasound
• Blood gas, lactate, renal function
• Coronary angiography if acute MI is suspected

Management

1. Treat the cause promptly
   • Urgent reperfusion with PCI is central in MI-related cardiogenic shock.
   • Correct unstable arrhythmias with cardioversion, pacing, or appropriate antiarrhythmic measures.
   • Urgent surgery may be needed for mechanical complications or severe valvular lesions.
2. Oxygen and ventilatory support
   • Treat hypoxemia.
   • Noninvasive ventilation may help cardiogenic pulmonary edema in selected conscious patients.
   • Intubation can worsen hypotension, so it needs careful preparation.
3. Fluids only if appropriate
   • Do not give large empiric fluid volumes to a patient with pulmonary edema.
   • A cautious fluid challenge can be considered in suspected right ventricular infarction or true hypovolemia, with close reassessment.
4. Vasopressors and inotropes
   • Norepinephrine is commonly used to restore perfusion pressure in severe hypotension.
   • Dobutamine may be used when cardiac output remains low after pressure is supported.
   • Choice depends on rhythm, blood pressure, and local critical-care/cardiology input.
5. Mechanical circulatory support
   • Selected patients may require temporary support, such as an intra-aortic balloon pump, Impella, or VA-ECMO in specialist centers.
   • Evidence and indication depend strongly on the cause of shock and patient selection. Recent reviews focus on this evolving area, including PMID 39661305.

---

4. Obstructive shock

Definition

Main causes

1. Cardiac tamponade
2. Tension pneumothorax
3. Massive pulmonary embolism
4. Less common:
   • Constrictive pericarditis
   • Aortic dissection obstructing flow
   • Air embolism
   • Fat embolism
   • Severe pulmonary hypertension in selected settings

A. Cardiac tamponade

Mechanism

Features

• Hypotension
• Raised JVP
• Quiet heart sounds: classic Beck triad, but all three are not always present
• Tachycardia
• Pulsus paradoxus
• Dyspnea
• Electrical alternans can occur on ECG
• Bedside echo: pericardial effusion with chamber collapse

Treatment

• Immediate pericardial drainage, usually pericardiocentesis or surgical drainage.
• Give cautious fluids only as a temporary measure while preparing definitive decompression.
• Do not delay drainage in unstable tamponade.

B. Tension pneumothorax

Mechanism

Features

• Sudden respiratory distress
• Severe hypoxemia
• Hypotension
• Unilateral reduced/absent breath sounds
• Hyperresonance on percussion
• Distended neck veins may occur
• Tracheal deviation is late and not required for diagnosis

Treatment

• Immediate needle or finger thoracostomy, followed by chest tube insertion.
• Do not wait for chest radiograph if the diagnosis is clinically likely in an unstable patient.

C. Massive pulmonary embolism

Mechanism

Features

• Acute dyspnea, chest pain, syncope, tachycardia
• Hypotension and shock
• Raised JVP
• Hypoxemia, though it can be normal
• Right-heart strain on ECG/echo
• Dilated, poorly functioning RV on echo

Treatment

• Oxygen and hemodynamic support
• Anticoagulation if no contraindication
• Systemic thrombolysis, catheter-directed therapy, or surgical embolectomy in high-risk PE with shock, depending on bleeding risk and available expertise

In obstructive shock, the key treatment is relief of the obstruction, not simply fluids or vasopressors.

---

5. Septic shock

Definition

Common sources

• Pneumonia
• Urinary tract infection or pyelonephritis
• Intra-abdominal infection
• Biliary infection
• Skin/soft tissue infection
• Meningitis
• Infected devices or catheters
• Postoperative infection

Pathophysiology

• Vasodilation from inflammatory mediators and nitric oxide
• Capillary leak and relative hypovolemia
• Endothelial dysfunction
• Microcirculatory impairment
• Myocardial depression in some patients
• Coagulopathy and microthrombi
• Cellular metabolic dysfunction

Features

• Fever or hypothermia
• Tachycardia and tachypnea
• Suspected or confirmed infection
• Warm extremities and bounding pulse early in some patients
• Cold, mottled limbs in late or severe shock
• Confusion
• Oliguria
• Elevated lactate
• Leukocytosis or leukopenia
• Thrombocytopenia and coagulopathy can occur

Investigations

• Blood cultures before antibiotics if this does not delay therapy
• Culture possible source material: urine, sputum, wound, CSF, etc.
• CBC, lactate, renal and liver function, coagulation profile
• ABG/VBG
• Imaging to locate source: chest imaging, ultrasound, CT when appropriate
• Bedside echocardiography if cardiac dysfunction or a competing shock type is suspected

Management: first hour priorities

1. Recognize sepsis and measure lactate
2. Take cultures rapidly
3. Give broad-spectrum IV antimicrobials promptly
   • Selection is based on likely source, local resistance patterns, allergies, immune status, and healthcare exposure.
4. Fluid resuscitation
   • Balanced crystalloid is often preferred.
   • Reassess frequently, especially in heart or kidney failure.
5. Vasopressor support
   • Norepinephrine is first-line when hypotension persists after initial fluid or when fluid is unsafe.
   • Initial MAP target is commonly 65 mmHg.
6. Source control
   • Drain abscess
   • Remove infected line
   • Operate for perforation, ischemic bowel, necrotizing infection, etc.
7. Consider vasopressin or epinephrine
   • If adequate MAP is not achieved with norepinephrine.
8. Consider dobutamine
   • If cardiac dysfunction and persistent hypoperfusion remain despite adequate pressure and volume.

---

6. Anaphylactic shock

Definition

Common triggers

• Foods: peanut, tree nut, shellfish, milk, egg
• Drugs: antibiotics, NSAIDs, anesthetic agents
• Insect stings
• Latex
• Exercise-associated reactions
• Contrast agents in some cases

Pathophysiology

• Peripheral vasodilation
• Increased vascular permeability and rapid intravascular volume loss
• Bronchoconstriction
• Mucosal edema
• Urticaria and angioedema

Features

Skin and mucosa

• Urticaria
• Itching
• Flushing
• Lip/tongue swelling
• Angioedema

Airway/breathing

• Hoarse voice
• Stridor
• Wheeze
• Dyspnea
• Hypoxemia
• Respiratory arrest in severe cases

Circulation

• Hypotension
• Tachycardia
• Dizziness/syncope
• Collapse

Gastrointestinal

• Abdominal cramps
• Vomiting
• Diarrhea

Management

1. Intramuscular epinephrine is first-line

• Give IM epinephrine into the anterolateral thigh immediately when anaphylaxis is suspected.
• Adult dose commonly used: 0.5 mg IM of 1 mg/mL solution, equivalent to 0.5 mL of 1:1000 solution.
• Repeat approximately every 5 minutes if symptoms persist, according to local protocol.
• Do not delay epinephrine for antihistamines, steroids, IV access, or tests.

2. Airway and oxygen

• Call for emergency help.
• Give high-flow oxygen.
• Prepare for early advanced airway management if voice change, stridor, tongue swelling, or rapidly worsening symptoms occur.

3. Circulation

• Lay the patient flat with legs elevated if tolerated.
• Avoid standing or walking.
• Give rapid IV isotonic crystalloid for hypotension.
• Refractory shock may require an IV epinephrine infusion in a monitored critical-care setting.

4. Adjuncts

• Inhaled beta-agonist for persistent bronchospasm.
• Antihistamines can improve itch/hives but do not treat airway obstruction or shock.
• Corticosteroids have delayed effects and must not replace epinephrine.

5. Observation and prevention

• Observe because biphasic symptoms can occur.
• Refer for allergy evaluation.
• Provide an epinephrine auto-injector and trigger-avoidance education where appropriate.

---

7. Neurogenic shock

Definition

Causes

• Acute cervical or high thoracic spinal cord injury, especially above T6
• Spinal anesthesia
• Severe brainstem injury, rarely

Pathophysiology

• Arterial vasodilation: low SVR and hypotension
• Venous pooling: reduced venous return and preload
• Unopposed vagal tone: bradycardia
• Impaired temperature regulation

Clinical features

• Hypotension
• Bradycardia or inappropriately normal heart rate, unlike most other shock states
• Warm, dry, flushed skin initially
• Peripheral vasodilation
• Hypothermia
• Weakness, sensory loss, or paralysis suggesting spinal cord injury
• Priapism may occur in acute spinal cord injury

Diagnosis

• Full spinal examination
• Neurologic deficits
• CT/MRI of spine when stable and indicated
• ECG and echocardiography if cardiac causes are possible
• FAST exam and imaging to exclude bleeding

Management

1. Spinal protection
   • Maintain immobilization and prevent secondary spinal injury.
2. Airway and ventilation
   • Cervical injury can impair diaphragm/intercostal function.
   • Monitor closely for respiratory failure.
3. Judicious fluids
   • Give enough fluid to correct associated hypovolemia, but avoid over-resuscitation.
4. Vasopressor
   • Norepinephrine is often preferred because it supports vascular tone and may assist heart rate through beta activity.
   • Target MAP should follow spinal-cord-injury protocol and specialist guidance.
5. Treat symptomatic bradycardia
   • Atropine may be used.
   • Severe/refractory bradycardia may need pacing or vasoactive support.
6. Temperature management
   • Prevent hypothermia.

---

8. Endocrine shock

Definition

1. Adrenal crisis
2. Myxedema coma
3. Thyroid storm, less commonly causing profound shock through cardiovascular collapse

A. Adrenal crisis

Causes

• Primary adrenal insufficiency, such as Addison disease
• Sudden cessation of long-term glucocorticoid therapy
• Pituitary or hypothalamic disease
• Adrenal hemorrhage
• Severe infection, surgery, or trauma in a patient with impaired adrenal reserve

Pathophysiology

• Reduced vascular responsiveness to catecholamines
• Vasodilation and refractory hypotension

• Sodium loss
• Hyperkalemia
• Dehydration and hypovolemia

Features

• Hypotension or shock
• Weakness, vomiting, abdominal pain
• Fever may occur
• Confusion
• Hypoglycemia
• Hyponatremia
• Hyperkalemia in primary adrenal failure
• Hyperpigmentation in chronic primary adrenal insufficiency

Management

• Do not wait for test results if adrenal crisis is suspected.
• Draw cortisol and ACTH if feasible without delaying treatment.
• Give IV hydrocortisone according to emergency protocol.
• Give isotonic IV fluid.
• Correct hypoglycemia and electrolyte disturbance.
• Treat precipitating infection or other trigger.

B. Myxedema coma

Definition

Features

• Altered mental state
• Hypothermia
• Bradycardia
• Hypotension
• Hypoventilation and carbon dioxide retention
• Hyponatremia
• Hypoglycemia
• Nonpitting edema, dry skin, coarse features
• A trigger is often present: infection, cold exposure, sedatives, stroke, heart failure, or surgery

Management

• ICU-level care
• Airway and ventilatory support as needed
• Passive rewarming
• IV thyroid hormone under endocrinology/critical-care guidance
• Empiric hydrocortisone until coexisting adrenal insufficiency is excluded
• Treat precipitating cause

C. Thyroid storm

Features

• Fever
• Severe tachycardia or atrial fibrillation
• Agitation/delirium
• Diarrhea and vomiting
• Heart failure
• Jaundice may occur

Management

• ICU care
• Beta-blockade only with caution, particularly if severe heart failure or shock is present
• Antithyroid drug, iodine at the appropriate interval, corticosteroid, cooling, fluids, and treatment of trigger

---

9. Traumatic shock

Definition

• Hemorrhagic shock
• Obstructive shock: tension pneumothorax, tamponade
• Neurogenic shock: spinal cord injury
• Cardiogenic shock: myocardial contusion, MI, arrhythmia
• Distributive/inflammatory shock from major tissue injury and later sepsis

Causes and mechanisms

• External or internal bleeding
• Chest trauma causing tension pneumothorax or tamponade
• Pelvic fracture causing massive occult hemorrhage
• Spinal cord injury causing neurogenic shock
• Crush injury and severe tissue damage
• Burns causing plasma loss
• Traumatic brain injury complicating resuscitation goals

Key assessment

Catastrophic hemorrhage

• Identify and control immediately with direct pressure, tourniquet, hemostatic dressing, or pelvic binder.

Airway with cervical spine protection

• Airway management while protecting the cervical spine.

Breathing

• Look for tension pneumothorax, open pneumothorax, massive hemothorax, flail chest.

Circulation

• Identify hemorrhage.
• Assess chest, abdomen, pelvis, long bones, and external wounds.
• Perform FAST/eFAST ultrasound in unstable trauma where available.

Disability and exposure

• Assess pupils, GCS, neurologic function, and full body surface for wounds.

Management

1. Control external hemorrhage.
2. Activate massive transfusion protocol when indicated.
3. Give early blood products rather than large crystalloid volumes in major hemorrhage.
4. Correct hypothermia and calcium deficits.
5. Urgently decompress a suspected tension pneumothorax.
6. Treat tamponade with surgical or pericardial intervention.
7. Provide urgent surgery or interventional radiology for internal bleeding.
8. Avoid permissive hypotension in significant traumatic brain injury. Brain perfusion must be maintained.
9. Reassess constantly because multiple shock mechanisms may coexist.

---

Quick comparison table

One-line memory aid

• Empty tank: hypovolemic
• Broken pump: cardiogenic
• Blocked circulation: obstructive
• Wide, leaky vessels: distributive
• Trauma: assume bleeding until proven otherwise
• Anaphylaxis: epinephrine first
• Neurogenic: hypotension with bradycardia after high spinal injury
• Adrenal crisis: fluids plus hydrocortisone immediately

Toxic Shock Syndrome (TSS)

• Staphylococcus aureus: staphylococcal TSS
• Streptococcus pyogenes (group A Streptococcus): streptococcal TSS, or STSS

---

Causes and risk factors

1. Staphylococcal TSS

• Tampon use, especially prolonged retention
• Vaginal packing or contraceptive diaphragms
• Postoperative wound infection
• Burns
• Skin abscesses
• Postpartum or post-abortion infection
• Nasal packing
• Osteomyelitis, arthritis, or other localized staphylococcal infection

2. Streptococcal TSS

• Cellulitis
• Deep soft-tissue infection
• Myositis
• Necrotizing fasciitis
• Postoperative wound infection
• Infection after a skin injury, chickenpox lesions, or childbirth

---

Pathophysiology

Toxin-producing S. aureus or group A Streptococcus
                    ↓
Superantigen toxin enters circulation
                    ↓
Massive, non-specific T-cell activation
                    ↓
Cytokine release: TNF, IL-1, IL-2, interferon, etc.
                    ↓
Vasodilation + capillary permeability + fluid leakage
                    ↓
Hypotension, tissue hypoperfusion, multiorgan failure

• Systemic vascular resistance: low
• Capillary leak: high
• Intravascular volume: relatively depleted
• Cardiac output: may be high early, low later due to myocardial depression
• Lactate: elevated due to impaired tissue perfusion

---

Clinical features

Early symptoms

• Sudden high fever, usually ≥38.9°C
• Chills, severe malaise, headache
• Muscle pain
• Nausea, vomiting, diarrhea
• Severe focal pain at a wound or limb can suggest deep streptococcal infection
• Dizziness, fainting, or weakness

Circulatory features

• Hypotension
• Tachycardia
• Poor urine output
• Confusion or reduced consciousness
• Shock and multiorgan failure

Skin and mucosal features

• Diffuse, red, sunburn-like rash: blanching erythroderma
• Red eyes, mouth, pharynx, or vagina
• “Strawberry tongue” may occur
• Skin peeling or desquamation, especially on palms and soles, often 1 to 2 weeks later

Organ involvement

Fever + hypotension + diffuse rash + multisystem involvement = suspect TSS.

---

Diagnosis

Key diagnostic work-up

• Blood cultures
• Culture from wound, vagina, tampon, surgical site, or other likely source
• CBC with platelet count
• Renal function, liver function, electrolytes
• Lactate and blood gas
• Creatine kinase
• Coagulation profile
• Urinalysis
• Imaging if deep soft-tissue infection, abscess, necrotizing fasciitis, or another source is suspected

Staphylococcal TSS clinical criteria

1. Fever ≥38.9°C
2. Hypotension
3. Diffuse erythrodermatous rash
4. Desquamation during recovery
5. Multisystem involvement

Streptococcal TSS

• Hypotension
• Multiorgan involvement
• Isolation of group A Streptococcus from a normally sterile site or appropriate clinical setting

---

Management

1. Immediate resuscitation

• ABCDE assessment
• Oxygen and ventilatory support if necessary
• Two large-bore IV lines
• IV crystalloid resuscitation, reassessed repeatedly
• Vasopressor support, usually norepinephrine, if hypotension persists
• Monitor urine output, lactate, blood pressure, ECG, oxygenation, and organ function

2. Remove the source

• Remove tampon, vaginal sponge, nasal pack, or foreign body
• Drain an abscess
• Remove infected devices where feasible
• Debride infected wound
• Explore urgently if necrotizing fasciitis or deep tissue infection is suspected

3. Antibiotics

• Clindamycin is commonly added because it suppresses bacterial toxin production.
• For confirmed/suspected STSS, penicillin plus clindamycin is a standard directed regimen.
• For suspected staphylococcal disease, MRSA-active treatment is needed until susceptibility results are available.

4. Intravenous immunoglobulin

5. Organ support

• Mechanical ventilation for respiratory failure/ARDS
• Dialysis for severe kidney failure
• Blood products for severe coagulopathy or bleeding
• Surgical amputation may rarely be necessary for uncontrolled necrotizing infection

---

Staphylococcal vs streptococcal TSS

---

Prevention

• Change tampons regularly and use the lowest absorbency necessary.
• Do not leave tampons in longer than recommended.
• Alternate with pads when feasible.
• Remove tampons immediately if fever, vomiting, diarrhea, rash, dizziness, or fainting develops.
• Keep wounds clean and seek care for increasing pain, redness, swelling, fever, or discharge.
• Follow postoperative wound-care advice.
• Seek urgent care for severe pain out of proportion to visible skin findings, especially with fever or rapidly worsening illness.

When to seek emergency help

• Fever with fainting, low blood pressure, confusion, or collapse
• A widespread red rash plus vomiting/diarrhea
• Sudden severe pain and swelling near a wound
• Fever and rapidly worsening illness after surgery, delivery, a skin injury, or tampon use
• Reduced urine output, breathing difficulty, or marked drowsiness