Six possible clinical problems occurring in the early postpartum period of cows:

 

Possible clinical problems occurring in the early postpartum period of bovines:

milk fever

PPH

Hypoglycemia(ketosis)

Downer cow syndrome

hypomagnesemia

udder edema

1.    Milk fever:

Milk Fever is also called Parturient Paresis

Definition

It is a febrile disease that occurs most commonly at/or after parturition (12-72 hours).

Etiology

It is caused by Hypocalcemia.

Epidemiology

It occurs in high producing cows 5-10 years.

Clinical Findings

A) Excitement stage:

·    Restlessness, hypersensitivity, tremor, and tetany.

·    Protrusion of tongue and grinding of teeth. Shaking of the head with a stiff gait.

B) Sternal Recumbancy:

·    Depression, drowsy, sternal recumbency, and unable to rise.

·    The head turned into the flank. Hypothermia with cool skin.

·    Decreased heart sounds and increased heart rate (180/minute).

·    Dry muzzle and eye, dilated pupil, ruminal stasis, secondary bloat, and constipation.

·    No anal reflex (anal relaxation).

C) Lateral recumbency:

·    Cows always comatose, lateral recumbency, and unable to set up.

·    Hypothermia and increase heart rate up to 120/minutes.

·    The animal dies after 12-24 hours.

Complication:

Hypomagnesemia, dystokia, and uterine prolapse

Treatment

·    Calcium borogluconate 25% (large cow 800 - 1000 cc & small cow 350 - 500 cc) half dose I/V and half-dose S/C. daily till recovery

·    Dexamethasone, 10 cc I/M, as corticosteroid drugs.

·    VITA-JECT, ADE3 5-10 cc I/M, as a single dose of vitamins.

·    Glucose 25% 2-3 L I/V daily, as a supportive treatment

2.Post parturent heamoglobonuria (Pph):

Postparturant hemoglobinuria is also called hypophosphotemia

Etiology

It is a metabolic disease of high producing dairy cows, usually occurring 2-6 weeks after parturition.

The diseases usually occur in buffaloes at the 5th -7th months of pregnancy.

It is caused by low phosphorus level in the blood resulting from low phosphorus intake either by ration or grazing on pasture for a long period of 3-4 months as berseem.

Clinical Findings

·    Anorexia, pica, and decrease of milk yield.

·    Hemoglobinuria, anemia, general weakness & pale mucous membrane associated with normal body temperature, finally jaundice and dehydration may occur.

·    In the terminal stage, gangrene and/or sloughing of the digit and tips. Ketosis and locomotion disturbances may develop.

·    Sometimes death occur due to anemic anoxia

Differential diagnosis

·    Babesiosis (fever, hemoglobinuria, tick on the animal, blood film)

·    bacillary hemoglobinuria

·    water intoxication

·    leptospirosis

·    urinary I tract affections (hematuria).

Treatment

·    Sodium Acid Phosphate or Sodium Dibasic Phosphate 20% (60 g dissolved in 300 ml DW to be given by I/V route)

·    followed by an S/c dose after 12 hours intervals for 3-5 days.

·    Also oral administration of 80 gm Sodium Acid Phosphate or 120 gm bone meal in the ration daily till complete recovery.

·    Catozal or Tonophosphane 50 cc I/M or I/V daily 3 - 5 days

·    Super-Phos (vitamin A & D, Iron, and phosphorous) 100 g orally daily/ week.

·    Glucose 25% for the treatment of ketosis. As supportive treatment.

 

3.Hypoglycemia (ketosis)

Definition and Causes

It is an impairment of the metabolism of carbohydrates and volatile fatty acids leading to intoxication from ketoses in the blood.

It is caused by hypoglycemia occurring in the first month of lactation in cattle.

Clinical Findings

A). Wasting form:

·    Decrease in appetite, milk production, and body weight.

·    Depression and disinclination to move and eat.

·    Decrease ruminal movement, but normal pulse, respiration, and temperature. Ketoses smell on the breath and milk.

·    Feces are firm and dry.

·    Woody cow due to wasting and loss of skin elasticity.

B). Nervous form:

·    The animal walks in circles and crossing the legs.

·    Appears Blind.

·    Vigorous licking of the skin

·    . Depraved appetite.

·    Hyperesthesia with moderate tremor and tetany.

·    Recurrent attack of nervous signs may occur 8-12 hours.

Treatment

·    Glucose 25% 1-2 liter I/V twice daily for 3 - 5 days.

·    Treacle and glycerol 0.5 -1 liter orally.

·    Predef 2X 10 cc I/M daily for 2 days (increase blood glucose).

·    Ca. D. Mg 500 ml I/VR/ Cobalt and B12 to (help in the proper metabolism of propionic acid.

4.Hypomagnesemia tetany

Definition and causes

It is a highly fatal disease of lactating cow and small ruminant, after parturition by two months. It is caused by hypomagnesemia. It occurs due to feeding grass

pasture low in magnesium content, grasses with high potassium content (cereal crops), pasture top dressing with nitrogen partial starvation, and recurrent diarrhea.

Clinical Findings

1.    Acute stage:

Sudden onset of anxiety, muscle tremor, ear twitch, hyperesthesia, staggering in gait, and easy falling.

Tetanic-clonic convulsions with opisthotonus.

Jaw champing, frothy salivation, and bellowing.

Protruded third eye-lid to cover most of the eyeball, and continuous movement of the eyeball.

The eyelid may be retracted.

Quite period between convulsions

. Hypothermia increases respiratory and heart rate. Response to treatment with magnesium solution I/V very good (untreated cases die after 30-60 minutes).

1.    Subacute stage:

·    Loss of appetite, suppressed rumination, and low milk yield.

·    Staggering in gait, muscular tremor.

·    Frequent defecation and urination.

·    Spontaneous recovery in few days.

1.    Chronic stage:

Gradual loss of condition, some sudden deaths, dullness, depressed milk yield.

The cow finally may pass into convulsions and dies unless prompt treatment is applied.

Differential diagnoses:

·    nervous form of ketosis

·    rabies

·    acute lead poisoning,

·    vitamin A deficiency

·    tetanus.

Treatment

·    Neurazine 3 ampoules in cattle & 1 ampoule in calf I/M. To handle the animal quietly before treatment.

·    Magnesium Sulfate (33 g in 500 ml DW), filter and sterilize before use (slowly I/V please follow heart and pulse rate).

·    This is followed by an S/C injection of 200 cc Magnesium Sulfate (25-30mg)

 

5.Downers cow syndrome

DEFINITION

A downer cow, defined as a cow that has been sternally recumbent for more than 24 hours, is not suffering from hypocalcemia, and has no obvious condition (e.g. mastitis, toxemia, or injury), is a common presentation in farm animal veterinary practice.

Etiology

·    The downer cow has a multifactorial primary etiology.

·    The most common causes are related to dystocia and milk fever.

·    Unless the initial cause of recumbency is promptly treated, pressure damage (also called compartment syndrome) develops due to the prolonged weight of the cow on its hindquarters.

Clinical signs

·    The typical downer cow is bright and alert with a normal appetite, rectal temperature, pulse, and respiratory rate.

·    Cows that cannot maintain sternal recumbency and fall into lateral recumbency are depressed or hyperaesthetic have a poor prognosis.

·    Cows that make repeated attempts to rise and can move about are often called 'creepers' or 'crawlers'.

DIFFERENTIAL DIAGNOSIS

·    Possible primary causes may include traumatic events such as:

·    pelvic fractures

·    sacroiliac luxation/subluxation

·    rupture of the gastrocnemius tendon and dystocia leading to ruptured uterus internal hemorrhage and exhaustion.

MANAGEMENT

Approximately half of all downer cows will get up in 4–7 days.

·    If the cow has been down for longer than 10 days, the prognosis is poor; however, it is not exceptional for a cow to be recumbent for 14–21 days then rise unaided.

·    The latter situation usually applies to beef cows' recumbent after dystocia, where the calf was 'hip locked.

·    Good husbandry is important.

 

·    A dry, clean comfortable lying area, either a deep-bedded straw pen or outside in a sheltered grass paddock, should be provided.

·    The cow must be turned every three hours to prevent pressure damage. Provision of ad-libitum good-quality food and fresh water should be ensured.

·    Administering either NSAIDs (e.g. flunixin meglumine, ketoprofen) or corticosteroids will reduce pain and tissue damage as well as improving demeanor and appetite.

·    Any underlying metabolic and/or toxaemic condition must be

treated.

6 .UDDER ODEMA

DEFINITION

This is a common problem affecting periparturient dairy cattle, especially heifers.

ETIOLOGY

Udder edema is a physiological phenomenon related to nutrition (high concentrate feeding, dietary sodium or potassium excess) and circulatory disturbance of udder vessels.

CLINICAL PRESENTATION

Animals are clinically normal except for hindlimb abduction when walking.

In severe cases, there is extensive pitting edema of the udder and teats extending to involve the ventral midline subcutaneous area.

Most cases resolve soon after calving when milking is initiated, but in severe cases treatment may be required.

DIFFERENTIAL DIAGNOSIS

Other causes of edema including cardiac failure mastitis.

DIAGNOSIS

Diagnosis is based on clinical findings of widespread edema.

MANAGEMENT

·    Milking can be started before calving.

·    edema can be greatly reduced following a corticosteroid injection

·    but this will also induce calving around 36 hours later.

·    Diuretic injections (e.g. frusemide)

and NSAIDs will aid elimination of edema