Respiratory acidosis develops because of decreased effective alveolar ventilation or breathing an atmosphere with elevated CO 2.
The initial buffering of the acid load produced by a respiratory acidosis is almost exclusively by the intracellular buffers. The principal ECF buffer, the bicarbonate-carbonic acid buffer pair, cannot buffer a respiratory acidosis. Carbon dioxide diffuses through the lung much more readily than O 2 ; thus, diseases that compromise ventilation normally result in decreases in p O 2 before significant increases in p CO 2 develop.
The respiratory center is extremely sensitive to minor changes in p CO 2 , and increased p CO 2 normally provides the major stimulus to ventilation Rose, In contrast, hypoxemia does not begin to promote enhanced ventilation until the arterial p O 2 is substantially decreased.
If, however, the arterial p CO 2 is held at normal values or is elevated because of intrinsic lung disease, then ventilation begins to be enhanced as the arterial p O 2 falls below 70 to 80 mmHg Rose, Any disorder that interferes with normal effective ventilation may produce a respiratory acidosis. The most common causes are primary pulmonary diseases ranging from acute upper respiratory obstruction, to pneumonia, to pneumothorax, and chronic obstructive lung disease. Diseases or drugs that affect the central nervous system may inhibit the medullary respiratory center and can produce a profound respiratory acidosis.
An additional cause of special importance in veterinary medicine is general anesthesia with volatile agents using a closed system. Under these conditions, ventilation may be seriously reduced without producing hypoxia. The high oxygen content of the gas mixture maintains high p O 2 in the blood, but depression of the respiratory center may result in insufficient alveolar ventilation so that CO 2 accumulates. This problem can be overcome through the use of a positive pressure ventilatory apparatus and careful monitoring of arterial blood gases during general anesthesia.
The compensating response for a respiratory acidosis is renal retention of bicarbonate and increased excretion of hydrogen ion. This response requires several days, and thus the response is seen only in a chronic respiratory acidosis.
In dogs with chronic respiratory acidosis, a compensating increase of 0. The extent of the rise in the plasma bicarbonate concentration in chronic respiratory acidosis is determined by increased renal hydrogen secretion Rose, Exogenous bicarbonate is unnecessary, and should bicarbonate be administered to patients with a respiratory acidosis, it would be excreted without affecting the final plasma bicarbonate concentration.
Metabolic alkalosis is characterized by an increase in pH and bicarbonate. Metabolic alkalosis occurs with some frequency in domestic animals and is commonly observed in association with digestive disturbances in ruminants. The development of a metabolic alkalosis requires an initiating process capable of generating an alkalosis and the additional factors that are necessary for maintaining the alkalosis Rose, Generation of a metabolic alkalosis can be due to excessive hydrogen loss, bicarbonate retention, or as a contraction alkalosis.
A contraction alkalosis occurs with reduction of ECF fluid volume resulting from a loss or sequestration of sodium and chloride containing fluid without commensurate loss of bicarbonate Garella et al. Excessive hydrogen ion losses can result in a metabolic alkalosis. The most common causes of increased hydrogen loss are gastrointestinal losses of chloride-rich fluids associated with vomiting in small animals Strombeck, or sequestration of chloride-rich fluid in the abomasum and forestomach of ruminants Gingerich and Murdick, b; McGuirk and Butler, Excessive renal hydrogen loss associated with mineralocorticoid excess, diuretic usage particularly the loop diuretics such as furosemide , and low chloride intake may cause or contribute to the generation of a metabolic alkalosis Rose, Most of these disorders are also associated with the development of significant sodium and chloride deficits and resultant decreases in effective circulating volume.
These deficits and the responses that decreased effective circulating volume induce are central features of the processes that maintain and perpetuate a metabolic alkalosis. Hydrogen loss from the ECF can also occur with hydrogen movement into the cells in response to potassium depletion Irvine and Dow, Excessive bicarbonate administration is an additional potential cause of metabolic alkalosis.
Most normal animals can tolerate large doses of bicarbonate, and excesses are rapidly eliminated by renal excretion Rumbaugh et al. However, patients with decreases in effective circulating blood volume or with potassium or chloride deficits may not tolerate a bicarbonate load because renal clearance of excess bicarbonate is likely to be impaired.
The factors that are responsible for the maintenance of a metabolic alkalosis all impair renal bicarbonate excretion.
These factors may include decreased glomerular filtration of bicarbonate seen in some types of renal failure. However, the most common factor is increased renal tubular bicarbonate resorption, which is associated with the renal response to decreases in the effective circulating fluid volume, potassium depletion, or chloride depletion Rose, Sodium resorption is enhanced in response to hypovolemia to help restore normal effective circulating fluid volume.
The maintenance of electroneutrality requires that sodium resorption in the proximal tubule must be accompanied by a resorbable anion such as chloride, whereas in the distal tubule, sodium resorption is associated with the secretion of a cation, usually hydrogen or, to a lesser extent, potassium.
The only resorbable anion normally present in appreciable quantities in the proximal tubular fluid is chloride. In a metabolic alkalosis, plasma bicarbonate is increased and chloride concentration is generally decreased as the result of disproportionately high chloride losses that result from vomiting, sequestration of gastric fluid Whitlock et al.
The relative lack of the resorbable anion, chloride, in the proximal tubule thus allows a larger amount of sodium to reach the distal tubule where the action of aldosterone enhances hydrogen loss into the tubular lumen in exchange for sodium.
The maintenance of effective circulating volume is so critical that the body chooses to maintain circulating volume by enhanced sodium resorption by whatever means necessary, even at the expense of extracellular pH.
Renal hydrogen excretion is directly linked with bicarbonate resorption. Thus, it is not possible to eliminate the excess bicarbonate, and the metabolic alkalosis is maintained Rose, This mechanism is the reason for the paradoxic acid urine seen in some patients with metabolic alkalosis Gingerich and Murdick, a, b; McGuirk and Butler, Hypokalemia is another factor that contributes to the maintenance of a metabolic alkalosis.
Hypokalemia is associated with an increase in intracellular hydrogen ion concentration. Increased renal tubular cell hydrogen ion concentration may enhance hydrogen secretion and thus bicarbonate reabsorption by the tubular cells. Chemoreceptors in the respiratory center sense the alkalosis, and the respiratory response to a metabolic alkalosis is hypoventilation resulting in an increase in p CO 2.
In dogs, the expected compensating response is an increase of p CO 2 of 0. Respiratory alkalosis is associated with an increase in pH and a decrease in p CO 2.
Respiratory alkalosis is due to hyperventilation, which may be stimulated by hypoxemia associated with pulmonary disease, congestive heart failure, or severe anemia. Hyperventilation may also be associated with psychogenic disturbances or neurological disorders that stimulate the medullary respiratory center such as salicylate intoxication or Gram-negative sepsis.
Respiratory alkalosis may be seen in animals in pain or under psychological stress. Hyperventilation may occur in dogs and other nonsweating animals as they employ respiratory evaporative processes for heat loss to prevent overheating Tasker, The initial compensating response to an acute respiratory alkalosis is a modest decline in ECF bicarbonate concentration as the result of cellular buffering.
Subsequent renal responses result in decreased ECF bicarbonate concentration through reduced renal bicarbonate reabsorption. These responses require 2 to 3 days for completion. The decline in bicarbonate is partially offset by chloride retention in order to retain electroneutrality. Thus, hyperchloremia and decreased p CO 2 may be associated with compensated respiratory alkalosis as well as compensated metabolic acidosis.
Compensating responses for chronic respiratory alkalosis lasting several weeks may actually be sufficient to return pH to normal. In dogs, anticipated renal compensation for a chronic respiratory alkalosis results in a decrease of bicarbonate of 0.
Mixed acid-base disorders occur when several primary acid-base imbalances coexist de Morais, a. Metabolic acidosis and alkalosis can coexist and either or sometimes both of these metabolic abnormalities may occur with either respiratory acidosis or alkalosis Nairns and Emmett, ; Wilson and Green, Evaluation of mixed acid-base abnormalities requires an understanding of the anion gap, the relationship between the change in serum sodium and chloride concentration, and the limits of compensation for the primary acid-base imbalances Saxton and Seldin, ; Wilson and Green, Clinical findings and history are also necessary to define the factors that may contribute to the development of mixed acid-base disorders.
The following are important considerations in evaluating possible mixed acid-base disorders:. Compensating responses to primary acid-base disturbances do not result in overcompensation. With the possible exception of chronic respiratory acidosis, compensating responses for primary acid-base disturbances rarely correct pH to normal.
In patients with acid-base imbalances, a normal pH indicates a mixed acid-base disturbance. A change in pH in the opposite direction to that predicted for a known primary disorder indicates a mixed disturbance. With primary acid-base disturbances, bicarbonate and p CO 2 always deviate in the same direction. If these parameters deviate in opposite directions, a mixed abnormality exists. Although mixed acid-base abnormalities undoubtedly occur in animals and have been documented in the veterinary literature, they are often overlooked Wilson and Green, An appreciation of the potential for the development of mixed abnormalities is essential for the correct interpretation of clinical and clinicopathological data, which would otherwise be quite confusing.
Care should be taken when evaluating suspected mixed acid-base abnormalities that sufficient time has elapsed so that anticipated compensating responses could have occurred de Morais, a.
Some investigators prefer to use the following formula:. Because most of the published data on the anion gap in animal species are the result of calculations using the second equation Eq. The anion gap is most useful in situations where the concentrations of phosphate and plasma proteins, particularly albumin, are within the normal range see Section V.
The anion gap for most species of domestic animals appears to be similar to that defined for human subjects i. However, there do appear to be significant differences in the normal rang of the anion gap of different species as indicated in Table Adrogue et al. Age-related changes in anion gap have been reported in horses Gossett and French, , with young foals having a significantly larger anion gap than adults.
Further experimental data will be necessary to more clearly establish the normal range for the anion gap of animals under varying conditions. The simple calculation of anion gap can be employed in the categorization of acid-base disorders with regard to potential causal factors and may serve as a prognostic guide in a variety of circumstances Bristol, ; Garry and Rings, ; Shull, Decreases in anion gap can be seen with increases in cationic proteins associated with polyclonal gammopathy or multiple myeloma.
Decreases in anion gap resulting from decreases in unmeasured anions occur most commonly with hypoalbuminemia and hyperchloremic metabolic acidosis, but they also may be noted with overhydration. The causal factors associated with a hyperchloremic metabolic acidosis with a normal to low anion gap can often be differentiated based on the serum potassium concentration. Hyperchloremic metabolic acidosis associated with gastrointestinal fluid losses from diarrhea or renal causes such as renal tubular acidosis most often manifests a hypokalemia Saxton and Seldin, ; Ziemer et al.
There are indications that changes in hydrogen ion concentration may alter protein equivalency and thus alter the anion gap in either an acidosis or alkalosis Adrogue et al. Dehydration and alkalosis are potential, but minor, causes of increased anion gap. Most commonly, elevations of anion gap are associated with the development of a metabolic acidosis in which there is an increase in anions, which are not routinely measured in the clinical laboratory.
This is called a high anion gap acidosis and may be associated with an accumulation of metabolizable acids as in a lactic acidosis associated with anaerobic exercise, grain overload, or hypovolemic shock or ketoacidosis resulting from diabetes or ketosis or with the accumulation of nonmetabolizable acids as in uremic acidosis or various intoxications see Table The presence of a metabolic acidosis with a high anion gap thus provides grounds to undertake a thorough investigation of disease processes capable of producing an accumulation of these unmeasured anions.
The anion gap also may be useful in the identification of mixed acid-base imbalances. When the change in the anion gap does not approximate the change in bicarbonate, a mixed metabolic acid-base imbalance should be suspected.
In cases of grain overload in herbivores, a large ion gap may be due to increased ECF levels of D-lactic acid, which is not detected by the usual assays for lactic acid because they detect only the L-isomer produced in mammalian metabolism. Either a special assay for D-lactate must be performed, or an increased level of D-lactate may be assumed based on history and other clinical data.
If respiratory disturbances can be eliminated, the metabolic component of acid-base balance is indicated by the bicarbonate concentration. The bicarbonate determined in this fashion will be decreased in a metabolic acidosis and increased in a metabolic alkalosis.
Estimates of bicarbonate are often provided in automated chemistry profiles. These determinations may indicate the metabolic acid-base status. However, if acid-base abnormalities are suspected, a proper blood gas evaluation should be undertaken. These values are mathematically derived from the measurements of blood pH and p CO 2 and provide an indication of the metabolic component of acid-base balance. It should be noted that the metabolic changes indicated by these parameters do not always reflect the primary acid-base imbalances but may represent compensating responses for primary respiratory disorders.
The buffer base indicates the sum of all the buffer anions in blood under standardized conditions. The standard bicarbonate is the plasma bicarbonate concentration that would be found under specific conditions, which eliminate respiratory influences on the values obtained. The base excess, which is sometimes considered as the base deficit when the value is negative, indicates the deviation of the buffer base from normal.
This derived value is often supplied in routine assessment of acid-base balance and is generally taken as an indication of the deviation of bicarbonate from normal. In an animal with a metabolic acidosis, the calculated base deficit provides a means of estimating the amount of bicarbonate required to correct acid-base balance to normal.
This estimate is calculated by multiplying the base deficit by the probable bicarbonate space which is variably estimated from 0. In newborn animals, the bicarbonate may be even higher, 0. The usual figure used is 0. This calculation provides only a crude guide to bicarbonate requirements, but it can be a useful step in the quantitative approach for correcting a serious primary metabolic acidosis.
Peter Stewart Stewart , was the first to describe a quantitative physiochemical approach to acid-base balance. In this approach, the acid-base status of the aqueous solutions of the body is determined not only by the Henderson-Hasselbalch equation but also by a series of seven other relationships, all of which could be represented by equations which must be satisfied simultaneously. Acid-base balance is determined by three independent variables: 1 strong ion difference [SID], 2 the partial pressure of CO 2 , and 3 the total concentration of nonvolatile weak acids [Atot], the principal component of which is the plasma proteins but also includes inorganic phosphate.
Bicarbonate and hydrogen ion concentration, and thus pH, are dependent variables determined by the independent variables listed here. Many of these early papers directed to animal species used the human values for Atot and K a, which may not be appropriate. Species-specific data are now available. The simplified strong ion model was developed from the assumption that plasma ions act as strong ions, volatile buffer ions , or nonvolatile buffer ions.
Plasma pH is determined by five independent variables: p CO 2 , strong ion difference, concentration of individual nonvolatile plasma buffers albumin, globulin, and phosphate , ionic strength, and temperature. The model has provided an in vitro method for determination of species-specific values for [Atot] and K a, which has been applied to the plasma of horses, dogs, cattle, pigeons, and humans Constable, ; Constable and []Stampfli, ; Stampfli et al. Strong electrolytes are completely dissociated in aqueous solution and chemically nonreactive.
The [SID] is simply the difference between the total concentration of strong cations sodium, potassium, and magnesium and the total concentration of strong anions chloride, sulfate, lactate, acetoacetate, and 3-OH-hydroxybutyrate. Because they are present in higher concentrations in the body fluids, sodium, potassium, and chloride are normally the principal determinants of [SID]. The [SID] is synonymous with buffer base as described by Singer and Hastings and, as such, can be considered as roughly equivalent to the metabolic component of the traditional approach to acid-base balance.
Abnormalities in p CO 2 are viewed in essentially the same manner in both the traditional and nontraditional approach to acid-base balance as described earlier. The contribution of plasma proteins to acid-base balance is not considered in the traditional approach to acid-base balance. The [Atot] in body fluids exists in both dissociated [A — ] and undissociated [HA] forms. A decrease in [Atot] because of hypoalbuminemia causes an alkalosis with an increase in bicarbonate, whereas hyperalbuminemia has the opposite effect.
Hypoalbuminemia is one of the most common causes of alkalosis in older human patients McAuliffe et al. Changes in A — associated with changes in albumin concentration also have a direct and frequently overlooked effect on anion gap.
Increases in A — result in an increase in anion gap, whereas decreases in A — cause a decrease in anion gap McAuliffe et al. Change in protein concentration may potentiate or ameliorate the effects of alterations in SID on acid-base balance. As an example, in a vomiting dog, the elevated plasma protein associated with dehydration may reduce the bicarbonate increase anticipated for a given change in chloride concentration and SID. Protein and inorganic phosphate remain within the normal range in many clinical situations, and acid-base balance is then largely controlled by changes in p CO 2 mediated by the respiratory system, whereas changes in [SID] are largely under the control of the kidneys.
Renal compensation for primary respiratory disorders and respiratory compensation for primary metabolic acid-base disturbances are thought to be similar in both the traditional and nontraditional approach. Precise quantification of the anticipated compensating responses to primary acid-base disturbances based on change in SID has not yet been determined. Vomiting in a dog; heavy sweat loss in an endurance horse; displaced abomasum in a cow; and the administration of the loop diuretic, furosemide, in a cat result in similar acid-base disturbances.
In each circumstance, a disproportionate loss of chloride relative to sodium results in a hypochloremia and an increase in [SID]. Correction of the alkalosis is brought about by the provision of chloride, generally as sodium chloride or potassium chloride, which results in a decrease in [SID] and thus a return of the dependent variables, bicarbonate and pH hydrogen ion , toward normal. A metabolic acidosis with a large base deficit is generally treated with sodium bicarbonate.
In the traditional approach, the calculated bicarbonate requirement is administered as sodium bicarbonate to replace the bicarbonate deficit, whereas in the strong ion approach, the sodium bicarbonate is administered to provide the strong cation, sodium, without a strong anion. Other metabolizable anions could be substituted for bicarbonate and achieve a similar effect.
In practice, both approaches work, but the rationale is substantially different. Calculation of SID is simple and provides useful insight in patients with metabolic acid-base disturbances. Factors that influence SID range from changes in free water, to sodium-chloride imbalances that result from excessive losses or disproportionate retention of sodium or chloride, to the accumulation of strong organic anions.
Organic acidosis can be produced by the accumulation of exogenous as well as endogenous organic anions. Examples of exogenous anions include salicylate, glycolate and formate associated with the ingestion of aspirin, ethylene glycol, and methanol, respectively.
Many of these endogenous and exogenous organic anions are not routinely monitored in the diagnostic laboratory. This situation can create problems when calculating the SID because the presence of these unmeasured strong anions may not be appreciated. Although the anion gap can be helpful, it does not always accurately predict the presence of these compounds.
More sophisticated mathematical methods have been suggested as a means for the detection of unmeasured anions the strong ion gap Constable et al. In animals with major changes in protein or albumin concentration, the primary concern must be a thorough investigation of the cause of the increase or decrease in protein. The acid-base consequences of change in protein and albumin concentration tend to be modest but are a potential source of confusion when evaluating acid-base data.
The traditional approach and the nontraditional or strong ion approach to acid-base balance each has its supporters, and discussion over the benefits and limitations of either approach has at times been strident. However, this need not be an either-or situation. Both approaches have proven useful to address practical problems in both research and medical settings. The traditional approach based on the Henderson-Hasselbalch equation is simpler, more user friendly, and more widely accepted.
Bicarbonate concentration estimates the severity of the acid-base disorder, but the strong ion approach may provide a better understanding as to why the bicarbonate is changing because it integrates acid-base and electrolyte disorders de Morais, The strong ion approach has been gaining acceptance from the critical care community, which finds it useful in the analysis of the complex fluid, electrolyte, and acid-base problems presented to intensive care units.
A number of computer programs adaptable to hand-held electronic devices have been developed and take some of the mathematical fear out of using the strong ion approach. Dietary factors, particularly the dietary cation-anion balance DCAB , have been extensively studied in cattle, swine, poultry, and horses. Diets with a high DCAB, such as alfalfa hay, have an alkalinizing effect and are an important factor in the alkaline urine of most herbivores. High grain rations tend to have a lower DCAB.
Manipulation of the DCAB has been employed to enhance milk yield in dairy cattle, to reduce the incidence and severity of gastric ulceration in swine, to decrease the incidence of milk fever in cattle, and to alter the urine pH and calcium balance in horses.
On the other hand, supplementation of the diet of late-term cattle with calcium chloride or ammonium chloride so as to lower the DCAB and have an acidifying effect has been shown to reduce the incidence of milk fever by enhancing the mobilization of calcium from the bone Block, As the application of these dietary practices becomes more widespread, it is essential that we appreciate the implications of dietary factors and electrolyte supplementation on mineral metabolism and acid-base balance Fredeen et al.
Sodium bicarbonate supplementation has been used as a prerace ergogenic aid in racehorses. Although experimental studies have often failed to detect a measurable performance benefit from sodium bicarbonate supplementation, practical experience suggests that some horses, particularly standardbreds, show marked improvement in race times.
Administration of any substance with intent to alter the performance is illegal in most racing jurisdictions. In many racing states, horses must meet specific guidelines for venous blood pH and bicarbonate or risk disqualification.
It is important to understand the difference between volume regulation and osmoregulation. Osmoregulation is governed by osmoreceptors influencing ADH and thirst, whereas volume disturbances are sensed by multiple volume receptors that activate effectors such as aldosterone. Antidiuretic hormone increases water resorption and therefore urine osmolality , but it does not affect sodium transport directly.
Aldosterone enhances sodium reabsorption but not directly that of water. Thus, osmoregulation is achieved by changes in water balance and volume regulation mostly by changes in sodium balance.
Water balance is achieved when water intake from all sources is equal to water output by all routes. Water is available as drinking water, as water content of feedstuffs, and as metabolic water derived by oxidative metabolism. Oxidation of 1g of fat, carbohydrate, or protein results in the production of 1. Water is normally lost from the body by four basic routes: urine, feces, insensible loss respiratory and cutaneous evaporation , and sensible perspiration sweat in some animal species.
Water intake and output may vary considerably from day to day, but normal animals are able to maintain water balance within remarkably narrow limits and, at the same time, maintain the critical interrelationship between water balance and electrolyte balance.
For human subjects, there are well-established normal values for water intake and output via various routes. Although there is a substantial amount of data on water balance for many domestic animals English, a; Fonnesbeck, ; Hinton, ; Kamal et al. The symptoms and signs are set in boldface type as paragraph heads. These are clues to the pathophysiology of each disease which is important for accurate diagnostic hypotheses.
The key symptoms are commonly chief complaints. The clinician should be familiar with the diseases and syndromes summarized in the last subsection. The signs are placed in approximate order as they are encountered during the head-to-foot physical exam. When particular symptoms and signs are useful in differentiating between the various etiologies, they are discussed after the DDX: notation. Some findings are both a symptom and a sign.
In these instances, the finding is discussed where it most commonly occurs: vomiting is most often a symptom, though it can be witnessed; tenderness, although noted by the patient, is a sign elicited Your MyAccess profile is currently affiliated with '[InstitutionA]' and is in the process of switching affiliations to '[InstitutionB]'.
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Received: November 23, Published: December 4, Citation: Obrowski M, Obrowski S. Hyperemesis gravidarum—a serious issue during pregnancy: in-depth clinical review and treatment modalities. MOJ Womens Health. DOI: Download PDF. Hyperemesis gravidarum 1 is the medical condition of extreme, persistent nausea and vomiting during pregnancy. It is a serious complication of pregnancy that is characterized by intractable nausea, vomiting and dehydration.
It is estimated to affect 0. This serious condition, if left unchecked, can lead to dehydration, weight loss, and electrolyte imbalances. Hyperemesis gravidarum differs from Morning Sickness. The cause of this nausea and vomiting during pregnancy, which usually subsides after the first trimester, is believed to be related to the rapidly rising blood level of a hormone called Human Chorionic Gonadotropin HCG.
HCG is released by the placenta. There are numerous theories regarding the cause of Hyperemesis gravidarum, but the cause s remains controversial. It is thought that Hyperemesis gravidarum is due to a combination of factors which may vary between women and include: genetics, 2 obesity a major factor , body chemistry and overall health. It can also be life-threatening if not treated due to severe electrolyte imbalances that occur from severe, continuous vomiting.
Also, unlike morning sickness, Hyperemesis gravidarum can last throughout the pregnancy and usually comes with constant vomiting, but always with constant nausea.
A small percentage of patients with Hyperemesis gravidarum rarely vomit, but the nausea still causes most if not all of the same issues that Hyperemesis gravidarum with vomiting does. When Hyperemesis gravidarum is severe or inadequately treated, regardless of the reason, it may result in the following symptoms:. Although the pathophysiology of Hyperemesis gravidarum is poorly understood, the most commonly accepted theory suggests that levels of hCG are associated with it.
Hyperemesis gravidarum is a diagnosis of exclusion. Women experiencing Hyperemesis gravidarum are often dehydrated and lose weight despite efforts to eat. Although Hyperemesis gravidarum is usually easily established by taking a thorough history and physical exam, do not miss any of the following possible differentials:. Infections usually accompanied by fever or associated symptoms Urinary Tract Infection.
Gastrointestinal disorders usually accompanied by abdominal pain Gastroenteritis. Fetal status: Many fetuses demonstrate evidence of asphyxia and hypoxia; therefore, close monitoring of fetal status is necessary, along with the ability to expedite delivery should fetal compromise be evident.
Maternal coagulation status: Due to coagulation abnormalities that can accompany AFLP, patients may need to have replacement of their coagulation factors should cesarean delivery be necessary. Likelihood of success with induction of labor: If delivery cannot be safely accomplished within 24 hours from the time of diagnosis, then a Caesarean Section is mandatory.
Management of severe hypoglycemia: Necessary to avoid coma and death. Blood glucose should be monitored closely until hepatic function returns and the patient tolerates a regular diet. Renal function: can also be affected by several factors, including maternal hemorrhage, which can lead to acute tubular necrosis and hepatorenal syndrome.
Fluid balance should be closely monitored, as patients may develop pulmonary edema due to low plasma oncotic pressures. Metabolic Thyrotoxicosis Hyperthyroidism Graves-basedow disease: named after the Irish Physician Robert Graves and the German Physician Karl von Basedow who described several cases in and It was actually first described by Parry a few years earlier.
In all countries it is also known as "Thyrotoxicosis". The disease has a genetic component, although not every member of the afflicted families will suffer this condition. It is more common in females than in males.
It is caused by an abnormal protein called the thyroid stimulating antibody. This antibody stimulates the thyroid gland to produce large amounts of thyroid hormone in an uncontrolled manner. In normal people, the production of the thyroid stimulating antibody and other abnormal antibodies is prevented by a surveillance system. This system consists of certain blood cells called suppressor and helper lymphocytes, Killer Cells and other constituents.
Common symptoms include weight loss, nervousness, irritability, intolerance to hot weather, excessive sweating, shakiness, and muscle weakness. Other signs include a rapid pulse, loss of body fat, loss of muscle bulk, thyroid enlargement goiter , fine tremors of the fingers and hot, moist, velvety skin.
The eyes, which bulge from their sockets can be red and watery and the lids are swollen. Often the eyes do not move normally because the swollen eye muscles are unable to work precisely and patients can experience double vision. Thyroid hormones: have a wide variety of effects on the body and the signs and symptoms reflect these.
All the metabolic processes are "speeded up". Pulse rate is rapid over bpm and occasionally irregular atrial fibrillation Bowel function is increased diarrhea Sweat glands work excessively, causing the patient to often complain of hyperhidrosis.
The nervous system is also stimulated so that the patient becomes irritable and nervous. Despite an increase in appetite, the patient usually loses weight because food intake cannot keep up with the increased breakdown of body proteins. The end result is a thin, hot, nervous patient with bulging eyes and goiter - a classical clinical situation quickly recognized by any medical practitioner who has previously seen such a patient. Since the end result of this problem is an over stimulation of thyroid function, treatment of the symptoms requires blocking thyroid hormone production with antithyroid drugs, destroying the thyroid cells with radioactive iodine or surgically removing the thyroid gland thyroidectomy.
Radioactive iodine: Although radioactive iodine is by far the simplest and most convenient treatment, its use in younger adults and children has previously been a matter of concern because of the possible harmful effects of radiation. Radioactive iodine has been used for over 40years and there is no known evidence of any harmful effects.
Its use in adolescents is increasing. However, it occasionally aggravates the eye sight and preventive treatment with corticosteroids is sometimes warranted. Radioactive iodine is usually given in the form of a capsule. The dose is calculated from the size of the goiter and the 24hour iodine uptake obtained by performing a "Thyroid Uptake Test. Antithyroid drugs: Antithyroid drugs such as Propylthiouracil and Methimazole are commonly used in children and adults under the age of It may also be used at any age so as to bring about remissions, or prior to ablation therapy.
Therefore most patients require additional treatments. In addition, a very small percentage suffer side effects that very rarely can be severe liver problems, low white blood cell count. Because of the recent evidence of side effects of Propylthiouracil on liver function, especially in children, the FDA has issued a warning for its use. Propylthiouracil is still the treatment of choice during pregnancy since there is unclear evidence about Methimazole side effects in the fetus aplasia cutis, choanal atresia.
It is preferable to treat the hyperthyroidism before considering pregnancy. Another medication that can be given to treat the symptoms of hyperthyroidism is Propranolol or other beta-blockers.
This drug blocks the effects of excess thyroid hormones on the heart, blood vessels, and nervous system, but has no direct effect on the thyroid gland. It is contraindicated in patients with asthma. The occurrence of diabetic ketoacidosis in pregnancy compromises both the fetus and the mother.
It usually occurs in the later stages of pregnancy and is also seen in newly presenting Type 1 Diabetic Patients. Despite improvement in its incidence rates and outcomes over the years, it still remains a major clinical problem since it tends to occur at lower blood glucose levels and more rapidly than in non-pregnant patients often causing delay in the diagnosis.
DKA in pregnancy most commonly occurs in women with pregestational, insulin dependent diabetes who are poorly controlled or in women newly diagnosed with insulin dependent diabetes. DKA may be provoked by an exposure to a stress such as infection, surgery, or labor. Antibiotics: Antibiotics were discussed earlier in this report. The main reason to mention it here again briefly, is to NEVER give unnecessary antibiotics and to carefully choose which one is being prescribed if an antibiotic is absolutely necessary.
When a woman is pregnant, she will need about twice the amount of iron as she normally did before becoming pregnant. The body uses iron to make extra blood for your baby.
Eating iron-rich foods and taking extra iron approximately 30 mg. The human body uses iron during pregnancy to make extra hemoglobin for the mother and the fetus.
Getting enough iron can prevent a condition of too few red blood cells that can make you feel tired, called iron deficiency anemia. Having anemia can cause your baby to be born too small or too early. Advise your patient to eat a healthy diet during pregnancy, which can lessen the effects of morning sickness and Hyperemesis gravidarum.
Prescribe your patient with a good Prenatal Vitamin, numerous ones are available depending on where you live. Prescription Prenatal Vitamins are preferred in lieu of OTC Vitamins as the prescription vitamins are specifically formulated for pregnant patients.
Prenatal vitamins contain many vitamins and minerals. All of them contain folic acid, iron, iodine, and calcium which are especially important during pregnancy. Folic acid helps prevent neural tube birth defects, which affect the brain and spinal cord. Complete molar pregnancy: An egg with no genetic information is fertilized by a sperm. It does not develop into a fetus but continues to grow as a lump of abnormal tissue that looks a bit like a cluster of grapes and can fill the uterus.
Partial molar pregnancy: An egg is fertilized by two sperm. The placenta becomes the molar growth. Any fetal tissue that forms is likely to have severe defects.
A Molar Pregnancy causes the same early symptoms that a normal pregnancy does, such as a missed period or morning sickness. But a molar pregnancy usually causes other symptoms too, which may include:. A malignant, trophoblastic cancer, usually of the placenta. It is characterized by early hematogenous spread to the lungs.
It belongs to the malignant end of the spectrum in gestational trophoblastic disease GTD. It is also classified as a germ cell tumor and may arise in the testis or ovary.
Common investigations include blood urea nitrogen BUN and electrolytes, liver function tests, urinalysis and thyroid function tests. Hematological investigations include hematocrit levels, which are usually raised in Hyperemesis gravidarum.
An ultrasound scan may be needed to know gestational status and to exclude molar or partial molar pregnancy. Dry bland food and oral rehydration are first-line treatments. Due to the potential for severe dehydration and other complications, Hyperemesis gravidarum is treated as an emergency. If conservative dietary measures fail, more extensive treatment suchs as the use of antiemetic medications and intravenous rehydration may be required. If oral nutrition is insufficient, intravenous nutritional support may be needed.
For women who require hospital admission, thromboembolic stockings or low-molecular-weight heparin may also be used as measures to prevent the formation of a blood clot. IV hydration often includes supplementation of electrolytes as persistent vomiting frequently leads to not only a fluid deficiency, which can cause a patient to go into shock with a dropping blood pressure and an increased pulse rate but also severe electrolyte and vitamin deficiency.
Unfortunately, most patients do not seek treatment in the hospital or office until they are in trouble — so action must be taken quickly.
Supplementation for lost thiamine Vitamin B1 must be considered to reduce the risk of Wernicke's Encephalopathy, Vitamins A and B are depleted within two weeks and so extended malnutrition indicates a need for evaluation and supplementation.
In addition, electrolyte levels should be monitored and supplemented; of particular concern are sodium and potassium. The vitamins and supplements are sometimes available in 5 to 10 cc. Again, the clinical judgement and patient presentation are most important when utilizing any IV fluids for rehydration therapy.
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