Veterinary Medicine

General Systemic States

Topics covered:

Lesson 1: Hypothermia, Hyperthermia, Fever Lesson 2: Septicemia, Viremia Lesson 3: Toxemia and Endotoximea Lesson 4: Hypovolemic shock Lesson 5: Allergy and Anaphylaxis Lesson 6: Edema and acid-base imbalance Lesson 7: Pain and stress Lesson 8: Localized infections Lesson 9: Inappetence Lesson 10: Weight loss Lesson 11: Care of recumbent animals Lesson 12: Sudden and unexpected death

Hypothermia, Hyperthermia, Fever

Overview

Hypothermia: Body temperature below normal due to excessive heat loss or inadequate heat production.

Hyperthermia: Elevated body temperature due to failure of heat dissipation, not caused by a change in hypothalamic set point.

Fever: A regulated rise in body temperature resulting from pyrogenic mediators acting on the hypothalamic thermoregulatory center.

Pathophysiology

Hypothermia: Heat loss - heat production (neonates, anesthetized patients, environmental exposure).

Hyperthermia: Overheating (heat stroke, overexertion, confinement in hot conditions).

Fever: Release of cytokines (IL-1, IL-6, TNF-α) stimulates hypothalamus to reset body temperature higher.

Clinical Features

Hypothermia: Shivering, weakness, bradycardia, reduced reflexes, eventual coma.

Hyperthermia: Panting, tachycardia, collapse, seizures, organ failure.

Fever: Anorexia, lethargy, increased HR, dehydration, malaise.

Diagnosis

Rectal temperature measurement.

History (exposure, environment, illness).

CBC: leukocytosis (infection), dehydration markers.

Treatment

Hypothermia: Gradual rewarming (warm IV fluids, blankets).

Hyperthermia: Active cooling (cool water, fans, IV fluids). Avoid ice water (causes vasoconstriction).

Fever: Treat underlying cause (antimicrobials, anti-inflammatories, fluids).

Case Example

A newborn calf is found in a cold barn, unable to suckle and lying recumbent. Its rectal temperature is 34°C (normal approx 38.5°C). The calf is rewarmed with heat lamps, fed warm colostrum via tube, and gradually recovers.

Discussion Questions
  • How do you differentiate hyperthermia from fever in practice?
  • Why must hypothermia be corrected gradually instead of rapidly?
  • What physiological role does fever play in fighting infections?

Septicemia, Viremia

Overview

Septicemia: The presence of bacteria and their toxins in the bloodstream, leading to systemic illness.

Viremia: The presence of viruses in the bloodstream, either transient (during infection spread) or persistent (chronic infections).

Pathophysiology

Septicemia: Entry of bacteria (umbilicus in neonates, mastitis, pneumonia) > toxins > systemic inflammation > shock.

Viremia: Viral replication in host > release into bloodstream > dissemination to target tissues.

Clinical Features

Septicemia: Fever, tachycardia, injected mucous membranes, petechiae, depression, possible shock and death.

Viremia: Often asymptomatic early; may progress to systemic signs depending on virus (e.g., parvovirus causing enteritis, FMD causing vesicles).

Diagnosis

Septicemia: Blood culture, CBC (leukocytosis/leukopenia).

Viremia: PCR, serology, virus isolation.

Treatment

Septicemia: Broad-spectrum antibiotics, IV fluids, anti-endotoxin therapy.

Viremia: Supportive therapy (fluids, nutrition), antivirals where available (rare in livestock).

Case Example

A 5-day-old foal develops lethargy, fever, and diarrhea. Blood culture reveals E. coli septicemia. The foal is treated with IV fluids, antibiotics, and plasma transfusion, but prognosis remains guarded.

Discussion Questions
  • Why are neonates particularly susceptible to septicemia?
  • How does the presence of colostrum influence resistance to septicemia?
  • What are the main differences in clinical management between septicemia and viremia?

Toxemia and Endotoximea

Overview

Toxemia: Circulation of toxins (bacterial, fungal, chemical) in the bloodstream.

Endotoxemia: Specific form of toxemia caused by lipopolysaccharide (LPS) endotoxin from Gram-negative bacterial infections.

Pathophysiology

Toxins or endotoxins > widespread inflammation > cytokine release > vascular leakage, hypotension, organ dysfunction.

Endotoxemia commonly arises from Gram-negative mastitis, metritis, colic (horses), or GI diseases.

Clinical Features

Fever, tachycardia, injected mucous membranes (“toxic line”), diarrhea, shock, sudden death.

Diagnosis

Clinical signs plus history of bacterial infection.

CBC: leukopenia, toxic neutrophils.

Culture of source infection.

Treatment

IV fluids and electrolytes to correct shock.

NSAIDs (flunixin meglumine) to block inflammatory cascade.

Polymyxin B (binds endotoxin, used cautiously).

Treat underlying infection (antibiotics, surgery if needed).

Case Example

A high-producing dairy cow develops acute mastitis. Within hours, she becomes recumbent, with injected scleral vessels and cold extremities. Immediate aggressive IV fluids and flunixin are administered, but prognosis remains guarded.

Discussion Questions
  • How does endotoxemia differ from septicemia in terms of cause and progression?
  • Why is early recognition of endotoxemia critical for survival?
  • Which livestock species are most prone to endotoxemia, and why?

Hypovolemic shock

Overview

Hypovolemic shock is a life-threatening condition resulting from significant fluid or blood loss, leading to inadequate tissue perfusion.

Pathophysiology

Loss of intravascular volume (hemorrhage, diarrhea, dehydration).

Reduced venous return > decreased cardiac output > poor oxygen delivery > cellular hypoxia > organ failure.

Clinical Features

Tachycardia, weak or thready pulse.

Cold extremities, pale mucous membranes, prolonged capillary refill time (CRT).

Lethargy, collapse.

Diagnosis

History of trauma, diarrhea, or blood loss.

PCV/TP to assess dehydration/hemorrhage.

Blood lactate (marker of perfusion).

Treatment

Rapid IV fluid therapy (crystalloids, colloids).

Blood transfusion if hemorrhage.

Oxygen supplementation.

Address underlying cause.

Case Example

A dog presents after being hit by a car with visible bleeding and pale mucous membranes. Shock is diagnosed and treated with IV fluids and a blood transfusion. The source of hemorrhage is surgically corrected.

Discussion Questions
  • Why is rapid IV fluid administration crucial in hypovolemic shock?
  • How can PCV/TP help differentiate hemorrhage from dehydration?
  • Why does shock cause cold extremities?

Allergy and Anaphylaxis

Overview

Allergy: An exaggerated immune response to a normally harmless antigen.

Anaphylaxis: A severe, systemic allergic reaction that can be life-threatening.

Pathophysiology

Allergic reactions involve IgE antibodies triggering mast cell degranulation.

In anaphylaxis, widespread histamine release causes vasodilation, hypotension, and bronchoconstriction.

Clinical Features

Mild allergy: itching, urticaria (hives), swelling.

Anaphylaxis: dyspnea, collapse, tachycardia, vomiting/diarrhea, death.

Diagnosis

History of exposure (vaccine, drug, insect bite).

Rapid onset of signs.

Exclusion of other causes of collapse.

Treatment

Anaphylaxis: Epinephrine IM or IV immediately.

Supportive: Oxygen, IV fluids, corticosteroids, antihistamines.

Allergy: Antihistamines, corticosteroids, avoidance of trigger.

Case Example

A cow collapses within minutes of being given penicillin. Emergency epinephrine and IV fluids are administered, and the cow recovers after supportive care.

Discussion Questions
  • Why is epinephrine the first-line drug in anaphylaxis?
  • How does an allergic reaction differ from an anaphylactic reaction?
  • What preventive steps can be taken before administering vaccines?

Edema and acid-base imbalance

Overview

Edema: Abnormal accumulation of fluid in tissues.

Acid-base imbalance: Disturbances in blood pH due to respiratory or metabolic causes.

Pathophysiology

Edema: Caused by low plasma oncotic pressure (hypoproteinemia), increased hydrostatic pressure (heart failure), or lymphatic obstruction.

Acid-base:

  • Metabolic acidosis (diarrhea, ketosis).
  • Metabolic alkalosis (vomiting, abomasal displacement).
  • Respiratory acidosis (hypoventilation).
  • Respiratory alkalosis (hyperventilation).
Clinical Features

Edema: Swelling in dependent regions, brisket, ventrum, eyelids.

Acid-base: Weakness, altered respiration, neurologic signs.

Diagnosis

Edema: Physical exam, blood protein levels.

Acid-base: Arterial blood gas analysis, electrolyte testing.

Treatment

Edema: Treat underlying cause, diuretics if needed.

Acid-base:

  • Acidosis: IV bicarbonate.
  • Alkalosis: Correct chloride/potassium deficit.
  • Respiratory: Restore ventilation.
Case Example

A cow with severe Johne’s disease presents with ventral edema due to hypoproteinemia. Supportive therapy is initiated, but prognosis is poor.

Discussion Questions
  • Why does hypoproteinemia lead to edema?
  • How do you distinguish metabolic acidosis from respiratory acidosis clinically?
  • Why is treating the underlying cause more important than just correcting edema?

Pain and stress

Overview

Pain and stress negatively affect animal health, productivity, and welfare. Recognizing and managing them is critical in veterinary practice.

Pathophysiology

Pain: Nociceptors transmit stimuli to CNS.

Stress: Activation of hypothalamic-pituitary-adrenal (HPA) axis > cortisol release > immunosuppression, metabolic effects.

Clinical Features

Pain: Lameness, vocalization, reluctance to move, abnormal posture.

Stress: Restlessness, increased HR/RR, reduced productivity, suppressed immunity.

Diagnosis

Pain scoring systems (lameness score, grimace scales).

Behavioral observation.

Treatment

Pain: Analgesics (NSAIDs, opioids, local anesthetics).

Stress: Low-stress handling, adequate housing, minimize painful procedures.

Case Example

A dairy cow post-dehorning is restless, shaking her head, and off feed. Administration of NSAIDs improves comfort and feed intake.

Discussion Questions
  • Why is pain often underrecognized in livestock species?
  • How does chronic stress affect productivity?
  • What role does pain control play in animal welfare?

Localized infections

Overview

Localized infections are confined to one tissue or organ but may spread if untreated.

Pathophysiology

Bacteria invade locally > inflammation, pus formation.

May progress to systemic disease if barriers are breached.

Clinical Features

Swelling, heat, redness, pain, discharge.

Loss of function of affected organ/tissue.

Diagnosis
  • Physical exam.
  • Culture and sensitivity of discharge or tissue sample.
Treatment
  • Drainage of abscesses.
  • Local and systemic antibiotics.
  • Supportive care.
Case Example

A sheep develops a swollen jaw due to caseous lymphadenitis. The abscess is drained, and the area is disinfected. Antibiotics are used where appropriate.

Discussion Questions
  • Why is culture and sensitivity testing important in treating infections?
  • How do localized infections progress to systemic disease?
  • How can farm management reduce risk of localized infections?

Inappetence

Overview

Inappetence is reduced appetite and is a nonspecific but important clinical sign.

Pathophysiology

Can be caused by systemic illness, pain, fever, or stress.

Linked to altered hypothalamic regulation of hunger.

Clinical Features

Reduced feed intake, weight loss, depression.

Diagnosis

Thorough history and clinical exam.

Lab tests: CBC, chemistry, fecal analysis.

Treatment

Identify and treat underlying cause.

Nutritional support (tube feeding, IV glucose).

Appetite stimulants if necessary.

Case Example

A cow with pneumonia refuses feed for 3 days. Antibiotic therapy resolves infection, and appetite returns.

Discussion Questions
  • Why is inappetence a warning sign rather than a diagnosis?
  • How does prolonged inappetence affect rumen function?
  • What supportive measures can help maintain nutrition?

Weight loss

Overview

Weight loss is a chronic sign of disease or inadequate nutrition.

Pathophysiology

Results from reduced intake, poor absorption, increased metabolic demand, or chronic disease.

Clinical Features

Loss of body condition, poor growth, weakness.

Diagnosis

History, body condition scoring.

Fecal exam (parasites), blood work (chronic disease).

Treatment

Correct underlying disease.

Balanced nutrition, parasite control.

Case Example

A goat loses weight despite good feed. Fecal exam reveals heavy parasite burden, and deworming leads to recovery.

Discussion Questions
  • Why is body condition scoring important?
  • What is the difference between weight loss due to malabsorption vs. anorexia?
  • How do chronic infections cause weight loss?

Care of recumbent animals

Overview

Recumbency occurs when animals cannot rise, requiring intensive nursing care.

Pathophysiology

Causes: metabolic disease (hypocalcemia), trauma, neurologic disease.

Risk: muscle/nerve damage, pressure sores, pneumonia.

Clinical Features

Animal unable to stand.

Secondary complications from prolonged recumbency.

Treatment

Treat primary cause (IV calcium, surgery).

Supportive care: frequent repositioning, bedding, nutrition, hydration.

Case Example

A dairy cow with milk fever is recumbent. She receives IV calcium and supportive nursing care. She rises within hours.

Discussion Questions
  • Why must recumbent animals be repositioned frequently?
  • What secondary complications occur with prolonged recumbency?
  • What are key welfare considerations in recumbent animals?

Sudden and unexpected death

Overview

Death occurring without prior signs; requires thorough investigation.

Pathophysiology

Common causes: clostridial infections, acute poisoning, trauma, cardiovascular failure.

Clinical Features

Often none before death; carcass may show bloating, hemorrhage, or lesions on necropsy.

Diagnosis

Necropsy essential.

History (feed, environment, recent treatments).

Lab tests (toxicology, cultures).

Treatment

Prevention via vaccination, good nutrition, and biosecurity.

Case Example

A feedlot steer is found dead with no prior illness. Necropsy reveals clostridial enterotoxemia. Vaccination protocols are reviewed and updated.

Discussion Questions
  • Why is necropsy essential in cases of sudden death?
  • How can management prevent clostridial disease?
  • How does sudden death impact herd/flock health planning?