Eklampsia, when having a litter goes wrong
….or it could have been much worse
I was asked to report about my bad experience with a quite unusual eklampsia while the
whelping of my S-litter.
But let's start, when all begun
The mating…..
Mid October 24 Mia started her heat together with my 2 older girls Tonya and Kimi, a first
progesteron test at day 12 did read 3,5ng and I decided to start the next day to Austria. We
arrived Sunday evening and after a short visit at Rios home, we went to our hotel. Next day Mia
still wasn't very much interested in Rio, so I decided for another progesterone test, who showed
ovulation just occurred (11,8ng Mini-vidas) The next 2 days we got 2 slip matings, I managed to
hold them together for some minutes, next day no more interest from both sides, so now we just
could wait patiently.
23 days later, I could palpate at least 2 embryos, who were about the size of a walnut, so I
decided to cancel the ultrasound appointment.
Mia's pregnancy was without any abnormalities, she was her happy self, but started to become
huge quite early and I knew, we were going to get a bigger litter. The bigger she became, the
more she lost her appetite and probably the unbalanced diet, because she just did eat special
things, was the start of our story.
The whelping…..
started textbook like with a temperature drop while friday night, exactly 61 days after ovulation.
Hard contractions should start in about 12-24 hours, sometimes 36 hours after the drop and Mia
started with first mild labour sunday afternoon. Contracting became better, but still no puppy
after 4 hours, so I decided to call my vet, ultrasound showed, that the puppies are fine, so she
got medication to help with the extension of the cervix and we went back home. At 11 p.m.
finally the first little boy was out, unfortunately stillborn. After 2 hours without any more labour
signs, vet again and since it was after midnight, Mia was already exhausted, we decided for a c-
section. The ineffective labor was probably the first sign of low calcium, but of course we never
expected that outcome. C-section gave us 9 more puppies, I was busy to get them to breath,
but all 9 and Mia were well and we all went home at 4 a.m. for a bit of deserved sleep.
The day after…..
I slept for about 2 hours, Mia and the pups next to me in my bed , when I realised that
something is totally wrong with Mia. She didn't react, couldn't close her mouth and her jaws
were like stiffened, she couldn't stand nor walk and positional reflexes were like zero. Monday
was a holiday here in Germany, so while starting to panick, I tried to contact every vet nearby
and just, when I planned to rush to the next emergency clinic (1,5 hours driving), my vet called
back, he was of course still sleeping on his day off.
I started bottle feeding in the morning, so the babies were sleeping calmly in a warm box and I
flew to vet. Blood work showed way to low calcium levels and thanks god after fluid and calcium
infusion, she was able to walk again and looked so much better. So we rushed home again to
the other girls and the puppies. Kimi,my oldest girl, helped cleaning the puppies and I was bottle
feeding everyone again, Mia was still in frail condition and of course had zero milk. Next day vet
again, because she was still not eating, but she started to clean the babies.
My wonderful pack, day 3….
Tonya, who was in heat together with Mia gave birth to “her phantom puppies” while night and in
the morning she started to whine and tried to get as near as possible to Mia. I never separate
my mom's and Mia allowed Tonya to help, I still could cry, when I think about all. So the babies
were luckily having 3 moms now, Mia, Tonya and me…
I really feared to loose Mia, but she started slowly to get better, we have been at vet every day
for fluid and medication.
Two weeks later….
Mia is completely recovered, her milk came in and the puppies are fat and healthy with 2 moms
feeding them. And I finally could enjoy them too.
A bit of science…
Eclampsia in Small Animals
(Postpartum Hypocalcemia, Periparturient Hypocalcemia, Puerperal Tetany)
ByJean A. Hall, DVM, PhD, DACVIM, Department of Biomedical Sciences, Carlson College of
Veterinary Medicine, Oregon State University
Reviewed/Revised Jul 2022 | Modified Sept 2024
Eclampsia (periparturient hypocalcemia) is characterized by progressive neurologic
signs including tremors, ataxia, and disorientation; eventually followed by seizures,
coma, and death. It occurs most commonly in small-breed dogs that are nursing large
litters, especially at peak lactation, 2–3 weeks after whelping. Hypocalcemia may also
occur during parturition and may precipitate dystocia. A presumptive diagnosis is based
on signalment and clinical signs; confirmation requires measurement of serum calcium
concentration. A total serum calcium concentration < 7 mg/dL is confirmatory. Treatment
depends on the severity of neurologic signs but usually requires IV administration of
calcium gluconate.
Eclampsia is an acute, life-threatening condition that usually occurs at peak lactation,
2–3 weeks after whelping. Small-breed bitches with large litters are most often affected.
Hypocalcemia may also occur during parturition and may precipitate dystocia.
Etiology and Pathogenesis of Eclampsia in Small Animals
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 compensate for the efflux of
calcium via the mammary glands during lactation. Heavy lactational demands from large
puppies or a large litter are often noted. The incidence is higher in small breeds of dogs,
although eclampsia can occur in any breed, with any size of litter, and at any time during
lactation. Rarely, it occurs during late gestation in bitches. Although uncommon in
queens, hypocalcemia may occur during early lactation. In dogs, supplementation with
oral calcium during pregnancy may predispose the animal 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.
Inadequate production of parathyroid hormone (PTH) during the hypocalcemic crisis is
not responsible for eclampsia in dogs. In dairy cows with a similar condition, parturient
paresis, production of PTH is adequate; however, the pool of osteoclasts for PTH to
stimulate is not. The small osteoclast pool results from feeding a high concentration of
dietary calcium during the nonlactating period, which suppresses secretion of PTH by
the parathyroid gland and stimulates secretion of calcitonin by parafollicular C cells.
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. The
paresis observed in cattle, rather than the tetany evident in dogs, is probably results
from a combination of factors. Cows often have concurrent mild hypermagnesemia.
Magnesium is a calcium-channel antagonist and plays a key role in modulating any
activity governed by intracellular calcium fluxes. Cows also have increased volatile fatty
acids (which are inhibitory at neuromuscular synapses), and the threshold potential at
neuromuscular junctions is higher in cows than in dogs.
In dogs with hypocalcemia, unlike cows, 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 that 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 sodium channels is that calcium ions bind to
the exterior surfaces of the 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 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 of Eclampsia in Small Animals
Panting and restlessness are early clinical signs of eclampsia. Mild tremors, twitching,
muscle spasms, and gait changes (stiffness and ataxia) result from increased
neuromuscular excitability. Behavioral changes such as aggression, whining, salivation,
pacing, hypersensitivity to stimuli, and disorientation are common. Severe tremors,
tetany, generalized seizure activity, and finally coma and death may occur.
Hyperthermia may occur in severe cases. Prolonged seizure activity may cause
cerebral edema. Tachycardia, hyperthermia, polyuria, polydipsia, and vomiting
sometimes occur. Historically, the bitch has been otherwise healthy and the neonates
have been thriving.
Although hypocalcemia usually occurs postpartum, clinical signs can appear prepartum
or at parturition. Mild hypocalcemia may contribute to ineffective myometrial
contractions and slow the progression of labor without causing other clinical signs.
Heavy panting may produce a respiratory alkalosis. Ionized calcium is the
physiologically available fraction of calcium; it is affected by protein concentration, acid-
base status (alkalosis favors protein binding of serum calcium and will decrease blood
concentrations of the biologically important ionized calcium, thus exacerbating
hypocalcemia), and other electrolyte imbalances. Thus, the severity of clinical signs
may not correlate with total calcium concentration.
Diagnosis of Eclampsia in Small Animals
Presumptive diagnosis based on signalment and clinical signs
Confirmatory diagnosis based on results of measurement of serum calcium
concentration
Diagnosis is often based on signalment, history, clinical signs, and response to
treatment. A pretreatment total serum calcium concentration of <7 mg/dL in dogs or < 6
mg/dL in cats confirms the diagnosis; noting that reference values vary between
laboratories. However, in many cases IV treatment with calcium is started before serum
calcium concentration is known. A serum biochemical analysis is useful to exclude
concurrent hypoglycemia and other electrolyte imbalances. Prolongation of the Q–T
interval and ventricular premature contractions may be evident on an 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 concentration in a hypocalcemic animal is strongly suggestive of primary
hypoparathyroidism. A commercially available human intact-PTH assay has been
validated in both cats and dogs; PTH-calcium curves are also similar in cats and dogs.
Treatment and Prevention of Eclampsia in Small Animals
Guided by the severity of neurologic signs
Administration of IV calcium gluconate with appropriate monitoring
Slow intravenous administration of 10% calcium gluconate—0.5–1.5 mL/kg over 10–30
minutes (5–20 mL is a typical dose)—is an effective treatment for eclampsia, usually
resulting in clinical improvement within 15 minutes. Muscle relaxation should be
immediate.
During administration of calcium, heart rate should be carefully monitored by
auscultation or ECG for bradycardia or arrhythmias. Adverse effects resulting from too
rapid administration of calcium include bradycardia, shortening of the Q–T interval, and
premature ventricular complexes. If an arrhythmia develops, calcium administration
should be discontinued until the heart rate and rhythm are normal; then administration
can be resumed at half the original infusion rate.
It is important to base the dosage of calcium on a calculation of elemental calcium
because different products vary in the amount of calcium available. The dosage of
elemental calcium for hypocalcemia is 5–15 mg/kg, IV, slowly over 10 minutes. Calcium
gluconate, 10%, contains 9.3 mg of elemental calcium/mL. Calcium chloride, 10%,
contains 27.2 mg of elemental calcium/mL. Thus, for calcium gluconate, 10%, the
dosage is ~0.5–1.5 mL/kg, IV, slowly over 10 minutes; and for calcium chloride, 10%,
the dosage is ~0.18–0.55 mL/kg, IV, slowly over 10 minutes. Calcium gluconate solution
may be preferred over calcium chloride because the former is perceived to carry a lower
risk of tissue injury if inadvertent extravasation occurs.
Once the animal is stable, the dose of calcium gluconate needed for initial control of
tetany may be diluted in an equal volume of normal (0.9%) saline and given
subcutaneously every 8 hours to control clinical signs. (Calcium chloride cannot be
given subcutaneously.) Alternatively, 5–15 mg of elemental calcium/kg per hour can be
continued intravenously. This protocol effectively supports serum calcium
concentrations while waiting for oral vitamin D and calcium treatment to have effect.
Ideally, serum calcium concentrations should be maintained at>8 mg/dL. Serum calcium
concentrations of <8 mg/dL indicate the need to increase the dosage of parenteral
calcium, whereas concentrations of>9 mg/dL suggest that it be decreased. The aim of
longterm treatment is to maintain the serum calcium concentration at mildly low to low-
normal concentrations (8–9.5 mg/dL).
The bitch may remain nonresponsive after correction of hypocalcemia if cerebral edema
has developed. Cerebral edema, hyperthermia, and hypoglycemia should be treated, if
present. Fever usually resolves rapidly with control of tetany, and specific treatment for
fever may result in hypothermia.
It is best not to let puppies or kittens nurse for 12–24 hours after the bitch or queen is
treated for hypocalcemia. During this period, they should be fed a milk substitute or
other appropriate diet; if mature enough, they should be weaned. If tetany recurs during
the same lactation, the litter should be removed from the bitch or queen and either
hand-raised (<4 weeks old) or weaned (>4 weeks old).
After the acute crisis, elemental calcium at 25–50 mg/kg per day orally in three or four
divided doses is given for the remainder of lactation. Again, the dose of calcium is
based on the amount of elemental calcium in the product (eg, calcium carbonate tablets
contain 295 mg elemental calcium/1-g tablet). In dogs, the dosage is usually 1–4 g/day,
in divided doses. In cats, the dosage of calcium is ~0.5–1 g/day, in divided doses.
Longterm maintenance treatment with oral vitamin D and oral calcium supplementation
usually requires a minimum of 24–96 hours before an effect is achieved. Hypocalcemic
animals should, therefore, receive parenteral calcium support during the initial
posttetany period. Calcium carbonate is a good choice because of its high percentage
of elemental calcium, general availability in drugstores in the form of antacids, low cost,
and lack of gastric irritation. The dosage of calcium can be gradually tapered to avoid
unnecessary treatment; commercial pet food usually contains sufficient calcium to meet
the needs of dogs and cats. However, to avoid acute problems of hypocalcemic tetany,
oral calcium supplementation should continue throughout lactation.
Vitamin D supplementation is used to increase calcium absorption from the intestines.
The concentration of serum calcium should be monitored weekly. The dosage of 1,25-
dihydroxyvitamin D 3 (calcitriol) is 0.03–0.06 mcg/kg per day. Calcitriol has a rapid onset
of action (1–4 days) and a short half-life (<1 day). Iatrogenic hypercalcemia is a
common complication of this treatment. If hypercalcemia results from overdosage, it can
be rapidly corrected by discontinuing calcitriol. The toxic effects resolve in 1–14 days.
This is a much briefer period than that observed with the use of dihydrotachysterol (1–3
weeks) or ergocalciferol (vitamin D 2 ; 1–18 weeks).
Corticosteroids lower serum calcium and, therefore, are contraindicated. They may
interfere with intestinal calcium transport and increase urinary loss of calcium.
Owners should be warned that eclampsia is likely to recur with future pregnancies.
Preventive steps to consider in the bitch include feeding a high-quality, nutritionally
balanced, and appropriate diet during pregnancy and lactation; providing food and water
ad lib during lactation; and supplementing feeding of the puppies with milk replacer
early in lactation and with solid food after 3–4 weeks of age. Oral calcium
supplementation during gestation is not indicated and may cause rather than prevent
postpartum hypocalcemia. Calcium administration during peak lactation may be helpful
in bitches with a history of eclampsia.