Shock Pathophysiology, Diagnosis and Emergency Treatment

Posted on Feb 9, 2026 in Medicine & Health

Shock: Pathophysiology and Cascades

SHOCK:

Px: 1. Decreased perfusion and O2 delivery to cells. 2. Inadequate aerobic metabolism. 3. Results in Cascade I and II.

Cascade I: Cellular Response

  • Cells shift to anaerobic metabolism.
  • Increased CO2 production and accumulation of lactic acid.
  • Progressive decline in cell function.
  • If shock persists, irreversible cellular damage occurs.

Clinical Features, Tests and Causes

CFTestsCauses
  • Encephalopathy / altered mental status
  • Capillary refill > 3 s
  • Oliguria
  • Tachycardia
  • Tachypnea
  • Hypotension
  • Central venous pressure (CVP)
  • Lactate > 3 mmol/L
  • Base deficit < -4 mEq/L
  • PaCO2 < 32 mmHg
  • Fever —> septic shock
  • Chest pain —> cardiogenic pulmonary causes (MI, PE)
  • Abdominal pain —> pancreatitis, aortic aneurysm

Emergency First Aid and Later Management

I – First Aid:
  • Keep patient warm.
  • ABCs (Airway, Breathing, Circulation).
  • Control bleeding.
  • Provide respiratory assistance as needed.
 II – Later management:
  • Supplemental O2.
  • Intubation & mechanical ventilation when indicated.
  • Obtain IV access.
  • Infuse 0.9% saline solution (as appropriate).
  • Monitor parameters (hemodynamics, urine output, labs).
  • Treat the underlying condition.

Shock Types and Specific Treatments

Bleeding / HypovolemicDistributive / SepticCardiogenicObstructive
  • Surgical control of bleeding.
  • Fluid resuscitation / infusion therapy.
  • Blood products + crystalloids (RBCs, plasma).
  • Infuse 0.5–1 L boluses as initial resuscitation (per protocol).
  • Vasopressors when indicated.
  • Broad-spectrum antibiotics.
  • Find and control source of infection.
  • Surgical or procedural management when indicated.
  • Vasopressors; inotropes as needed.
  • Epinephrine in selected cases.
  • Pericardiocentesis (for tamponade).
  • Decompression of pneumothorax.
  • Other interventions as indicated (drainage, thrombolysis, surgical relief).

Septic Shock: Criteria and Treatment

Septic Shock!

CFInstrumental / Labs
  • SIRS criteria:
    • Temperature > 38 °C or < 36 °C
    • Heart rate > 90 bpm
    • Respiratory rate > 20 /min
    • WBC > 12,000 /mm3
  • Organ dysfunction.
  • CBC
  • Electrolytes
  • Creatinine
  • Lactate (assess lactic acidosis)
  • Arterial blood gas
  • Culture samples (blood / urine / wound)
Note: Hypotension does NOT improve despite fluid resuscitation in septic shock.

Septic Shock Treatment (Tx)

I – Restore organ perfusion:
  • IV fluid resuscitation + vasopressors as indicated.
  • Hemodynamic monitoring (CVP, urine output, lactate clearance).
 II – Broad-spectrum antibiotics (empiric by source):
  • Respiratory tract: cefuroxime; or ampicillin/sulbactam + gentamicin (as indicated).
  • Urinary tract infection (UTI): ceftriaxone or cefotaxime.
  • Central nervous system (CNS): ceftriaxone; or cefotaxime + ampicillin (for Listeria coverage when indicated).
  • Skin & soft tissue: cefazolin; or cefuroxime + metronidazole; or ampicillin + sulbactam.

Hypovolemic Shock: Causes and Treatment

Etiology:

  • Bleeding / trauma
  • Surgery
  • Increased fluid loss (dehydration, burns, etc.)

→ ↓ Intravascular volume (decreased intravascular volume)

TX (Treatment)

  1. Evaluation and rapid assessment.
  2. Find the source of bleeding and control it.
  3. Infusion therapy: initial boluses (example: 2–3 L of NaCl solution over 20–30 min when indicated; consider Ringer’s lactate per protocol).
  4. Transfusion: RBCs + plasma as needed.
  5. Supplemental O2 (mask) and oxygen therapy.
  6. Intubation if respiratory failure or airway protection required.

Hemolytic Uremic Syndrome (HUS)

Gx:

  • Often presents in children (emergency).
  • Common cause: E. coli (post-diarrheal HUS).

Px — Triad:

  1. Thrombocytopenia
  2. Hemolytic anemia
  3. Acute renal failure (uremia)
CF:
  • Pale
  • Jaundice
  • Petechiae / purpura
  • Hepatosplenomegaly
 Lab:
  • Hemolytic anemia (Hct < 30%)
  • Thrombocytopenia
  • Coombs test negative
  • PTT increased

HUS Treatment

  • Supportive care (fluids, monitoring).
  • Dialysis in acute renal failure cases.
  • Fresh frozen plasma if indicated.
  • Plasmapheresis in selected cases.

Rickets: Causes, Presentation and Treatment

Gx (Etiology):

  • Vitamin D deficiency due to decreased skin synthesis
  • Rapid growth (increased requirements)
  • Avoidance of sunlight
  • Nutritional deficiency
  • Decreased absorption of vitamin D

Calcium deficiency:

  • Low intake
  • Malabsorption

Phosphorus deficiency

Pathophysiology

Vitamin D3 is formed in skin and hydroxylated in the liver and kidney:

  1. Liver produces calcidiol (25-OH vitamin D).
  2. Kidney produces calcitriol (1,25-(OH)2 vitamin D).
  3. Calcitriol increases calcium and phosphate absorption from the intestine into blood.
  4. Calcitriol increases reabsorption of phosphate in the kidney.

Clinical Features (CF)

  • Bone and joint pain
  • Muscle weakness
  • Fractures
  • Harrison groove (diaphragmatic groove on the rib cage)
  • Bowed legs
  • Kyphosis (spine)
  • Rachitic rosary (costochondral beading)
  • Frog belly (protuberant abdomen)

Diagnosis (Dx)

  • Laboratory tests depend on cause (vitamin D, calcium, phosphate, alkaline phosphatase).
  • Acidosis may be present in some contexts.
  • Hypochromic iron deficiency may coexist.
  • Radiographic changes on X-ray (radius, ulna, other long bones).

Treatment (Tx)

  • Nutrition optimization (calcium and vitamin D rich diet).
  • Massage and physiotherapy as supportive care.
  • Exercise as tolerated and recommended.
  • Vitamin D supplementation:
    • Single large dose: 600,000 U (as indicated in severe deficiency per local protocol).
    • Or gradual replacement: 5,000 U daily for 2–3 months (per clinical judgment).
  • Calcium preparations as needed.