A couple of months ago, Charlie sent me a copy of a longer article that he had written about Hunting Dog Hypoglycemia. Great information, including some little known information about nutrition and fitness, but a little too long for a blog post. At my request, Charlie boiled it down to the following article. A big thank you to Charlie for this very valuable contribution...
Some Personal Observations, Opinions, Hypotheses, and a Little Science Concerning Hunting Dog Hypoglycemia (HDH)
by Dr. C.A. Hjerpe, DVM - Davis, California
Before discussing my personal observations of and opinions concerning hypoglycemia in hunting dogs, I will first offer some disclaimers, present my credentials and provide some definitions. First, I wish to emphasize that I am not and have never been a small animal specialist, and my personal observations and opinions are based on recollections that are not backed up with detailed, written records, and should not be regarded as “research”.
I graduated from Cornell University’s New York State College of Veterinary Medicine in 1958, worked in private, mixed species veterinary practices for 5 years, and was a professor of large animal medicine at the School of Veterinary Medicine, University of California, Davis, for 31 years, until retiring in 1994. During the last 14 years of my academic career, I also served as Director of the UCD Veterinary Medical Teaching Hospital. During the past 48 years, I have owned one Weimaraner, 2 English setters and more English pointers than I would be able to recall and enumerate (probably more than 100). I have field trialed with most of these pointers, and have always hunted with my field trial dogs.
I think it appropriate to begin this presentation with a short discussion of hypoglycemia. When veterinarians or physicians say that a dog (or cow or person) is hypoglycemic, we are saying that the concentration of glucose (a specific type of sugar compound) in the blood of that individual is below the normal range for blood glucose values in that species. For a dog, it means that the patient’s blood glucose concentration is less than 59.4 milligrams per deciliter (mg/dl).
Many different diseases of dogs may cause hypoglycemia, so hypoglycemia is not a disease or a diagnosis but, rather, a non-specific biochemical alteration of body fluids. Clinical hypoglycemia in a dog means that (1) the dog’s blood glucose concentration is below normal, and (2) at least some of the characteristic clinical manifestations that always accompany marked reductions in blood glucose values are also present. Since clinical hypoglycemia can be caused by a number of different diseases (especially liver diseases and pancreatic B-cell tumors) clinical hypoglycemia is also not a specific disease. However, when we specify that we are talking or writing about PRIMARY clinical canine hypoglycemia, people will know that we are referring to a dog that has:
(1) very low blood glucose values (below 50 mg/dl),
(2) accompanied by typical clinical manifestations (symptoms or signs) of low blood glucose values, and
(3) that no other primary diseases capable of causing hypoglycemia are present. This condition is usually associated with prolonged, vigorous exercise, and is generally referred to as exertional hypoglycemia or hunting dog hypoglycemia (HDH). During the remainder of this discussion, I will use only the latter term when referring to it.
Glucose is the primary energy source for most cells in the body. Glucose is liberated from food by the digestive processes, absorbed into the blood stream from the stomach and intestines, and transported to the liver by the portal blood circulation. Within the liver, glucose is converted to glycogen and stored within specialized cells called hepatocytes. In response to falling blood glucose concentrations and/or the metabolic requirements of other body cells for glucose, liver glycogen is converted back to glucose, and released back into the blood stream.
Current scientific knowledge of basic energy metabolism suggests the reason why an otherwise healthy dog develops HDH during hunting: the dog’s liver glycogen reserves were insufficient for maintaining normal blood glucose concentrations, during the period of vigorous exercise that preceded the clinical signs of the disease. This supposition is based mostly on extrapolation from basic research conducted in mice, rats, human beings and in cell cultures, as little or no actual research has been done using HDH affected dogs
C. CLINICAL MANIFESTATIONS OF HDH AND THEIR DEVELOPMENT AND PROGRESSION:
The characteristic progression of typical clinical manifestations of HDH is organized, below, into Six Stages, using my own classification system:
Stage 1: Whenever hypoglycemia develops while a dog is being hunted, the first physical or behavioral evidence of it will be a gradual onset of fatigue. However, it should be emphasized that, in the vast majority of instances in which fatigue becomes evident during hunting, hypoglycemia will NOT be the cause. In most cases, the dog is simply becoming physically exhausted and/or overheated, or is experiencing intestinal or stomach cramping. Nevertheless, any dog that appears to become fatigued while hunting should be carefully observed for the possible appearance of stage 2 symptoms.
Stage 2: In addition to fatigue, the dog begins to evidence incoordination and/or staggering. At this point, it is urgent that all physical activity immediately cease, and that either the dog be fed (its regular dog food) or a concentrated glucose source, such as:
(1) 50% glucose solution in water or,
(2) corn syrup, be administered by mouth.
If the dog won’t eat, and no of sources of glucose are available, the dog should be taken to a veterinary clinic without delay (even though it is true that some dogs, in this stage of HDH, if rested, will recover spontaneously, without any treatment at all).
Stage 3: In addition to stage 1 and 2 signs, muscular tremors and spasms may occur, which may result in abnormal postures. The dog may be unable to open its mouth, or chew food that is offered, or may be unable to swallow food that is placed in its mouth. At some point during this stage, the dog may be unable to walk or stand without assistance. During this stage, it may be inadvisable to attempt to force-feed food or oral glucose supplements, because (if the patient cannot swallow) they may be inhaled and cause fatal inhalation pneumonia. It has been stated that glucose can be absorbed through the oral membranes, and that simply rubbing glucose on the gums can be effective treatment. This method of treatment seems suspect to me, and needs to be evaluated under controlled laboratory conditions, before I could recommend it. However, there is no harm in doing this, so long as it is done while the dog is being rushed to a veterinary clinic.
Stage 4: In addition to stage 1, 2 and 3 signs, the dog may begin having seizures/convulsions. This is very serious, because the dog may not be able to breathe during convulsions, may die of asphyxia during prolonged convulsions or, at the very least, may sustain permanent brain damage as a result of low levels of oxygen in the blood flowing through the brain during convulsions. From this stage on, an affected animal can only be effectively treated by a skilled and knowledgeable veterinarian in a well-equipped veterinary facility. The patient will require continuous intravenous drip infusion with 5% glucose in water, periodic monitoring of blood glucose values, and specialized equipment for correcting hypothermia and maintaining the body temperature within normal limits.
Stage 5: The dog is completely unconscious and unresponsive, a condition which is referred to as coma. Either the convulsions have ended, or the dog has passed directly from Stage 3 to Stage 5, without stopping in Stage 4. Dogs may recover completely when treated in Stage 5, or they may recover but have permanent brain damage, either from:
(1) the anoxia accompanying the convulsions in Stage 4, or from
(2) a prolonged period of severe hypoglycemia during stage 5.
Stage 6: This stage is death, which may occur in untreated animals as a result of exposure (and hypothermia) or, in either treated or untreated animals, as a result of severe damage to the brain and/or other vital organs from hypoglycemia and/or anoxia.
D. SOME PERSONAL OBSERVATIONS AND OPINIONS CONCERNING HDH:
I have personally observed and dealt with approximately 21 cases of HDH, all in my own pointers. About 10 cases occurred during foot hunting, one case occurred during horseback training, and the remainder occurred while I was conditioning dogs by “roading” them in harnesses from an all terrain vehicle (ATV). Of these 21 cases, only one terminated fatally, and only 2 required treatment in a veterinary clinic or hospital. Both of these latter cases made rapid and complete recoveries. All 3 of these severe cases were precipitated by roading. The remaining 18 cases were successfully managed by terminating their physical activity (when Stage 2 signs became evident) and either administering oral glucose solutions and/or feeding them.
I do not recall any cases of HDH occurring in my own dogs after they were 3 years of age. Most of my affected dogs were less than 2 years of age. Other authors have reported that dogs affected with HDH at a young age will (usually) become less susceptible to it with increasing age. Intact male and female pointers appear equally susceptible to HDH.
On 4 different occasions, I have observed HDH occurring (during exercise), shortly after my dogs were subjected to extreme chilling, as a result of being thoroughly drenched with cold water. My hypothesis is that the chilling effect of the cold water may (sometimes) trigger an unidentified physiological mechanism that impairs the release of glucose from the liver glycogen reserves, and might involve reductions in arterial blood flow to the liver. It is well known that vigorous physical exercise can shunt the flow of arterial blood away from the digestive tract and into the musculature and cardiopulmonary circulation. Cold water chilling might simply facilitate or accentuate this physiological phenomenon. Three of these 4 incidents occurred during roading. The 4th incident occurred during foot hunting, was my first experience with HDH, and is described below:
I was hunting with 3 dogs, during the morning of the opening day of pheasant season. After I had been hunting for about an hour, a cold rain began falling and, within 15 minutes, all 3 dogs began to stagger. Within a few more minutes, 2 of the 3 could no longer stand up. In addition to the chilling effect of the rainfall, I now know that these 3 dogs were also predisposed to HDH by my nutritional program: I had been feeding the least expensive dog food available from my local Safeway supermarket, and I had been observing that the less of it I fed to my dogs, the better they would run. So, as I progressively fed less to my dogs, they ran progressively better, but also became progressively thinner. It is also likely that their liver glycogen reserves were being progressively depleted. So when it started to rain that Saturday morning, and as my dogs became wet and chilled, all those “chickens” suddenly came home to roost.
I have seen no conclusive evidence that HDH is ever inherited, and I have owned only 3 dogs that were affected with HDH more than once. One dog that I am currently field trialing has been affected twice (to date), each time while being roaded. I also recall 2 other dogs that were each affected 3 times, always while being foot hunted. In virtually every instance in which one of my dogs has been affected with HDH, my dog was NOT the problem. I was the problem! If I had been a little smarter, a bit more “on the ball”, and not so willing to “cut corners” with my feeding and conditioning programs, nearly every one of the cases in my own dogs could have been avoided. In light of these observations, it makes little sense to me to cull a dog, simply because it has been affected with HDH on one or 2 occasions.
E. PREVENTING HDH:
In order to prevent HDH, the problem areas that need to be addressed (in approximate order of importance) are: (1) physical conditioning, (2) feeding, and (3) nutrition and ration formulation:
1. Physical Conditioning: Most of the HDH cases in my own dogs have occurred when I roaded or foot hunted them for periods of time that were excessively long, considering the physical condition that they were in at the time. Often these affected dogs had been in top physical condition only 10 to 20 days previously, but in the interim they had not received sufficient exercise to maintain their fitness. I appreciate that most hunters do not have the time and facilities required to insure that their dogs will always be in top condition when they want to go hunting with them. Consequently, it should come as no surprise to them when their dogs develop HDH, and they should always be prepared to effectively deal with it. All other things being equal, the more vigorously a dog hunts and the longer that dog is hunted, the greater will be its risk for developing HDH.
2. Feeding: When hunting dog people sit down together to talk about conditioning their dogs, they will almost always be thinking and talking about an exercise regimen that will result in the degree of cardiopulmonary fitness and muscular strength that their dogs must have in order to be good, strong hunters. However, there is another aspect to conditioning that is mostly “flying under the radar”, that few people know about, and which is almost never discussed. That aspect involves conditioning dogs so as to maintain large liver glycogen reserves, and to become primarily dependent upon those reserves as an energy source, and as a source of glucose for maintaining normal blood glucose concentrations. Ideally, a conditioning and feeding program for a hunting dog should seek to achieve the following end point objective: The dog should have achieved sufficient physical strength and cardiopulmonary and metabolic fitness that it is able run and hunt industriously for the entire length of the hunt, and be able accomplish this on an empty stomach.
It is generally recommended that hunting dogs be fed once each day, in late afternoon or early evening. This practice, which essentially starves your dog for 24 hours after each feeding, makes it IMPOSSIBLE for your dog to rely entirely on glucose entering the blood stream from the gastrointestinal tract for maintenance of normal blood glucose levels. As a result, your dog is FORCED to gradually increase its liver glycogen reserves, and adjust to using those reserves as the primary source of glucose for maintaining normal blood glucose levels.
After a hunting dog has been adequately conditioned for the work that will be expected of him/her, it should not be necessary to alter the feeding program that is being used, except (possibly) to increase the amounts fed so as avoid inordinate weight loss in dogs that are being hunted frequently for long periods of time. All other things being equal, a dog that is excessively thin will tend to be more prone to develop HDH than a dog that is in moderate to moderately thin condition. A fat but well-conditioned dog may be less prone to develop HDH than a thin dog, but is also more likely to become overheated and fatigued while hunting, especially during warm weather.
If a dog is fed a heavy meal shortly before being hunted, the dog may be slower and more sluggish than usual, and may experience gastrointestinal cramping and/or or vomiting during the hunt. However, I sometimes take advantage of this phenomenon, by purposely feeding a heavy meal to especially fast and wide-ranging dogs, just before I intend to foot hunt with them. Feeding dogs immediately before hunting them may even help to prevent HDH, so long as you adhere to the practice of feeding no more than one meal per day, and observe a 24-hour period between feedings.
In addition, if you have an ordinary hunting dog, one that is not in top physical condition and may be at risk to HDH, it is not going to do any harm to carry some dry dog food with you, and to feed your dog a bit from time to time, while you are actually hunting. This latter practice has been widely recommended for preventing HDH when hunting with poorly conditioned dogs.
3. Nutrition and Ration Formulation: Basic biomedical research has demonstrated that liver glycogen storage can be greatly increased by feeding diets that contain only SMALL proportions of carbohydrates, especially small proportions of simple carbohydrates (like simple sugars and starches). In contrast, when diets containing LARGE proportions of simple carbohydrates were fed, it was found that liver glycogen reserves declined precipitously, and the animals came to rely heavily on gastrointestinal absorption of glucose for maintenance of normal blood glucose concentrations. Simple carbohydrates are rapidly digested to glucose in the gastrointestinal tract, and this glucose is rapidly absorbed into the blood stream. When these animals with low liver glycogen reserves (on high carbohydrate diets) were fasted and/or subjected to exercise, they were much more prone to develop hypoglycemia than were animals with high liver glycogen reserves (on low carbohydrate diets).
Thus, at least in theory, the risk of developing HDH in hunting dogs should be lessened by feeding rations that provide the smallest possible fraction of total ration calories in the form of carbohydrates, and the largest possible fraction of total ration calories in the form of proteins and fats. Since a high proportion of total ration nutrients fall into these 3 categories (carbohydrates, proteins and fats), the carbohydrate fraction will usually be lowest in those rations that contain the largest proportion of the other two macronutrient classes combined (protein plus fat).
The combined crude protein, crude fat and carbohydrate content of a “performance” dog food will account for approximately 85% of ration ingredients, by weight. For example, Purina’s Pro Plan Performance Formula dog food contains 30% crude protein, 20% crude fat, 12% moisture, 1.8% oleic acid, 0.9% calcium and 0.7% phosphorus. When you add up all these percentages and subtract the total from 100, you will have calculated the percentage of carbohydrates in the product, which is 34.6%. So, 34.6% (carbohydrates) plus 30% (protein) plus 20% (fat) equals 84.6%. However, since we, as consumers, can not know the digestibility and biological availability of all of the proteins, fats and carbohydrates included in this (or any other currently available) dog food product, it is not possible for us to calculate the precise proportion of ration calories provided by each of these 3 major nutrient classes. Nevertheless, we can probably help to minimize our problems with HDH by feeding a premium, dry, performance dog food that contains a high combined percentage of crude protein and crude fat.
I cannot recommend any of the dietary carbohydrate supplement products that are currently being marketed to dog owners for purposes of “rapidly replenishing muscle and liver glycogen reserves following strenuous exercise”. The use of these products in dogs (as opposed to use in people and horses) would be tantamount to feeding a high carbohydrate diet, which would be counterproductive to our objective (which is to reduce carbohydrate intake and force our dogs’ bodies to increase glucose synthesis from proteins and fats for purposes of increasing liver glycogen reserves, and to rely on those reserves as the primary source of glucose for body functions).
F. THE BARE MINIMUM THAT EVERY HUNTER SHOULD KNOW ABOUT HDH:
Hunters who remember and consistently follow the 2 recommendations listed below, should never have to pay a veterinary bill for a dog with HDH, much less have to bury one that dies of it:
1. Hunters should always carry a half-pint of corn syrup (or other concentrated source of glucose) in a pocket of their hunting coat or vest. Should your dog become fatigued while hunting, watch him/her closely, and if he/she begins to appear weak or to stagger, stop all physical activity with that dog for that day, administer a couple of ounces of corn syrup by mouth, and feed him/her heavily as soon as possible (in other words, don’t wait to feed your affected dog until you normally feed your other dogs). For all practical purposes, (1) 50% glucose solution (in water), (2) corn syrup (which contains 100% glucose), (3) high fructose corn syrup (which contains 50% glucose and 50% fructose), (4) honey (which contains 50% glucose and 50% fructose) and (5) 100% natural fruit juices (with no artificial sweeteners) are all equally effective for oral treatment of HDH.
2. Hunters should also be aware that, on rare occasions, a dog that does not show either stage 1 or stage 2 clinical signs while hunting, may suddenly become severely hypoglycemic, shortly after the end of the hunt. Consequently, even though your hunting has ended and your dog is safely in a box, on a stakeout or in a kennel, your responsibility for the welfare of your dog does not end at that point. You must force yourself to remember to check on your dog 3 more times, at 10, 20 and 30 minutes after the end of the hunt, and be certain that he/she is behaving normally at those times.
Addendum by Dr. Hjerpe regarding feeding dogs prior to running or hunting...