Postpartum Hypocalcemia, Periparturient Hypocalcemia, Puerperal Tetany, Eclampsia

1. NAME :AMEER HAMZA
CLASS# 01
DVM FINAL YEAR
(SEMESTER:09)
SEC:A
SESSION:2016-2020
MEDICINE CLINIC 3
ASSIGNMENT SUBMITTED TO :
DR HAQ AMAN ULLAH
Assignment No.3
Describe in detail the etiology, pathogenesis, and treatment
of following diseases:
1. Eclampsia in dogs
Postpartum Hypocalcemia , Periparturient
Hypocalcemia , Puerperal Tetany , Eclampsia
Puerperal hypocalcemia is an acute, life-threatening condition usually seen at peak lactation,
2–3 wk after whelping. Small-breed bitches with large litters are most often affected.

2. Hypocalcemia may also occur during parturition and may precipitate dystocia.
Etiology:
Hypocalcemia most likely results from loss of calcium into the milk and from
inadequate dietary calcium intake. This imbalance in calcium metabolism occurs
because calcium mobilization from bone into the serum pool is insufficient to
maintain the efflux of calcium leaving through the mammary glands. Heavy
lactational demands from large puppies or a large litter are often noted. The incidence
is increased in small breeds of dogs, although puerperal hypocalcemia can occur in
any breed, with any size litter, and at any time during lactation. Rarely, it occurs
during late gestation in bitches. In dogs, supplementation with oral calcium during
pregnancy may predispose to eclampsia during peak lactation, because excessive
calcium intake during pregnancy causes downregulation of the calcium regulatory
system and subsequent clinical hypocalcemia when calcium demand is high.
Pathogenesis:
Inadequate production of parathyroid hormone (PTH) during the hypocalcemic crisis
is not responsible for eclampsia in dogs.. The small osteoclast pool results from
feeding a high level of dietary calcium during the nonlactating period, which
suppresses parathyroid gland secretion of PTH and stimulates parafollicular C-cell
secretion of calcitonin. Hypocalcemia at parturition interferes with the release of
acetylcholine at the neuromuscular junction, which is normally mediated by
extracellular calcium entering presynaptic nerve terminals through voltage-gated
calcium channels and triggering the fusion of acetylcholine-filled synaptic vesicles
with the presynaptic nerve terminus.

3. In dogs with hypocalcemia, excitation-secretion coupling is maintained at the
neuromuscular junction. The low concentration of calcium in the extracellular fluid
has an excitatory effect on nerve and muscle cells, because it lowers the threshold
potential (voltage level at which sodium channels become activated) so it is closer to
the resting membrane potential. With hypocalcemia, sodium channels become
activated (opened) by very little increase in membrane potential from their normal,
negative level. Therefore, the nerve fiber becomes highly excitable, sometimes
discharging repetitively without provocation rather than remaining in the resting state.
The probable way that calcium ions affect the sodium channels are that calcium ions
bind to the exterior surfaces of sodium channels. The positive charge of these calcium
ions alters the electrical state of the sodium channel protein, thus altering the voltage
level required to open the sodium channel. Because of the loss of stabilizing
membrane-bound calcium ions, nerve membranes become more permeable to sodium
ions and require a stimulus of lesser magnitude to depolarize. Tetany occurs as a
result of spontaneous repetitive firing of motor nerve fibers. Hypoglycemia can occur
concurrently.
Clinical Findings:
1.Panting
2.Restlessness
3.Mild tremors, twitching, muscle spasms, and gait changes (stiffness and ataxia)
result from increased neuromuscular excitability.
4. Behavioral changes such as aggression, whining, salivation, pacing,
hypersensitivity to stimuli, and disorientation are frequent
5. Severe tremors, tetany, generalized seizure activity, and finally coma and death
may be seen.
6.Hyperthermia may occur in severe cases.
7.Prolonged seizure activity may cause cerebral edema.
8.Tachycardia, hyperthermia, polyuria, polydipsia, and vomiting are sometimes seen.
Although hypocalcemia usually occurs postpartum, clinical signs can appear
prepartum or at parturition. Mild hypocalcemia (serum calcium concentration >7
mg/dL but below the normal reference range) may contribute to ineffective
myometrial contractions and slow the progression of labor without causing any other
clinical signs.

4. 9. Heavy panting may produce a respiratory alkalosis. Ionized calcium is the
physiologically available fraction; it is affected by protein concentration, acid-base
status (alkalosis favors protein binding of serum calcium and will decrease blood
levels of the biologically important ionized calcium, thus exacerbating hypocalcemia),
and other electrolyte imbalances.
Diagnosis:
Diagnosis is often made from the
1. History,
2. Clinical signs,
3. Response to treatment
A serum chemistry profile is useful to exclude concurrent hypoglycemia and other
electrolyte imbalances. Prolongation of the QT interval and ventricular premature
contractions may be seen on the ECG.
Differential diagnoses
include other causes of seizures such as hypoglycemia, toxicoses, and primary
neurologic disorders such as idiopathic epilepsy or meningoencephalitis.
Other causes of irritability and hyperthermia such as metritis and mastitis should also
be excluded.
If the parathyroid glands are functioning normally, serum PTH will be increased in
the face of hypocalcemia. Low or undetectable serum PTH in a hypocalcemic animal
is strongly suggestive of primary hypoparathyroidism .
Treatment :
1. Slow IV administration of 10% calcium gluconate is given to effect (0.5–1.5
mL/kg over 10–30 min; 5–20 mL is the usual dose). This usually results in rapid
clinical improvement within 15 min. Muscle relaxation should be immediate.
2.After the acute crisis, elemental calcium at 25–50 mg/kg/day in three or four
divided doses is given PO for the remainder of the lactation. Again, the dose of
calcium is based on the amount of elemental calcium in the product (ie, calcium
carbonate tablets contain 295 mg elemental calcium/1 g tablet). In dogs, the dosage is
usually 1–4 g/day, in divided doses.

5. 3. Longterm maintenance therapy with oral vitamin D and oral calcium
supplementation usually requires a minimum of 24–96 hr before an effect is
Vitamin D supplementation is used to increase calcium absorption from the
The concentration of serum calcium should be monitored weekly. The dosage of
1,25-dihydroxyvitamin D (calcitriol) is 0.03–0.06 mcg/kg/day. Calcitriol has a rapid
onset of action (1–4 days) and short half-life (<1 day).
Prevention:
Feeding a high-quality, nutritionally balanced, and appropriate diet during
pregnancy and lactation, providing food and water ad lib during lactation, and
supplemental feeding of the puppies with milk replacer early in lactation and with
solid food after 3–4 wk of age.
 Provide a high-quality, nutritionally balanced diet with a proper calcium and
phosphorus ratio during pregnancy and lactation. The optimal ratio of calcium to
phosphorus is 1.2 to 1
 It's often recommended to give oral calcium supplementation to the mom
immediately after whelping and continuing throughout lactation. This is especially
important during peak milk production
 Providing food and water as often as desired during lactation can also help
prevent eclampsia.
 Calcium supplementation should be avoided during pregnancy unless
otherwise advised by your veterinarian. This is because calcium supplementation
can affect the body's ability to regulate calcium, which increases the risk of
developing eclampsia. Knowing when to give calcium supplements to dogs (and
when not to) is essential
The puppies may need to be supplemented with a milk replacer early in lactation, and
they should be weaned as early as possible.