7
D iabetic ketoacidosis (DKA) is a common endocrine emergency in veteri- nary medicine. DKA results in acute metabolic derangement in dogs and cats, requiring prompt medical treatment. The nursing management approach to patients with DKA is similar to that of patients with other serious illnesses. Veterinary technicians must have a basic un- derstanding of the disease as well as the ability to perform various diagnostic and therapeutic procedures. Knowledge of the disease process and possible outcomes will enable technicians to anticipate and identify potential complications. Pathophysiology Diabetic ketoacidosis, which is a life-threatening complication of diabetes mel- litus (DM), is characterized by hyperglycemia, ketosis, acidosis, dehydration, and electrolyte imbalances. Hyperglycemia and ketoacidosis occur during insulin de- ficiency or resistance. Consequently, glucose and ketoacids are overproduced and underused. Despite the onset of hyperglycemia, cellular starvation occurs. Cell energy requirements that are not met stimulate gluconeogenesis (see the Glos- sary) and increased hepatic glycogenolysis. As a result, the animal’s body breaks down fat and protein stores to meet the energy requirements of cellular metabolism. Because the body is unable to keep up with the rate of production of this alternative energy source, ketone bodies accumulate in the blood. Eventually, hyperglycemia exceeds the renal threshold for glucose resorption and glucosuria, causing osmotic diuresis. Osmotic diuresis results in losses of sodium, potassium, phosphorus, magnesium, and body water. Increased water loss leads to severe dehydration and hypovolemia. Nausea, anorexia, and vomiting oc- cur when ketonemia and hyperglycemia stimulate the chemoreceptor trigger zone, further contributing to dehydration. Dehydration decreases tissue perfusion, caus- ing lactic acid production and exacerbating the existing acidosis (Figure 1). Assessment History and Risk Factors Although DKA occurs mostly in dogs or cats with previously undiagnosed DM, the condition may also develop in previously diagnosed diabetics with the same predisposing factors or in animals in which insulin has been administered improperly. Veterinary patients may have a history of polydipsia, polyuria, and weight loss. The acute presentation may include the sudden onset of anorexia, depression, abdominal pain, weakness, and vomiting. Many of the precipitating factors seen in humans may also contribute to DKA in animals. These risk fac- Endocrine Emergency— Diabetic Ketoacidosis Harold Davis, BA, RVT, VTS (Emergency and Critical Care) KEY POINTS Diabetic ketoacidosis is characterized by hyperglycemia, ketosis, acidosis, dehydration, and an electrolyte imbalance. The initial physical examination should focus on hydration status, central nervous system involvement and/or depression, and any coexistent conditions. The goals of therapy are to correct dehydration, restore intravascular volume, normalize blood glucose levels, and correct electrolyte and acid–base abnormalities. 14 Vol. 22, No. 1 January 2001 Peer-Reviewed CE Article #1

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Page 1: Endocrine Emergency— Diabetic Ketoacidosis · Diabetic ketoacidosis (DKA) is a common endocrine emergency in veteri- nary medicine. DKA results in acute metabolic derangement in

Diabetic ketoacidosis (DKA) is a common endocrine emergency in veteri-nary medicine. DKA results in acute metabolic derangement in dogs andcats, requiring prompt medical treatment.

The nursing management approach to patients with DKA is similar to that ofpatients with other serious illnesses. Veterinary technicians must have a basic un-derstanding of the disease as well as the ability to perform various diagnostic andtherapeutic procedures. Knowledge of the disease process and possible outcomeswill enable technicians to anticipate and identify potential complications.

PathophysiologyDiabetic ketoacidosis, which is a life-threatening complication of diabetes mel-

litus (DM), is characterized by hyperglycemia, ketosis, acidosis, dehydration, andelectrolyte imbalances. Hyperglycemia and ketoacidosis occur during insulin de-ficiency or resistance. Consequently, glucose and ketoacids are overproduced andunderused. Despite the onset of hyperglycemia, cellular starvation occurs. Cellenergy requirements that are not met stimulate gluconeogenesis (see the Glos-sary) and increased hepatic glycogenolysis. As a result, the animal’s body breaksdown fat and protein stores to meet the energy requirements of cellularmetabolism. Because the body is unable to keep up with the rate of production ofthis alternative energy source, ketone bodies accumulate in the blood.

Eventually, hyperglycemia exceeds the renal threshold for glucose resorptionand glucosuria, causing osmotic diuresis. Osmotic diuresis results in losses ofsodium, potassium, phosphorus, magnesium, and body water. Increased water lossleads to severe dehydration and hypovolemia. Nausea, anorexia, and vomiting oc-cur when ketonemia and hyperglycemia stimulate the chemoreceptor trigger zone,further contributing to dehydration. Dehydration decreases tissue perfusion, caus-ing lactic acid production and exacerbating the existing acidosis (Figure 1).

AssessmentHistory and Risk Factors

Although DKA occurs mostly in dogs or cats with previously undiagnosedDM, the condition may also develop in previously diagnosed diabetics with thesame predisposing factors or in animals in which insulin has been administeredimproperly. Veterinary patients may have a history of polydipsia, polyuria, andweight loss. The acute presentation may include the sudden onset of anorexia,depression, abdominal pain, weakness, and vomiting. Many of the precipitatingfactors seen in humans may also contribute to DKA in animals. These risk fac-

Endocrine Emergency—Diabetic Ketoacidosis

Harold Davis, BA, RVT, VTS(Emergency and Critical Care)

KEY POINTS

n Diabetic ketoacidosisis characterized byhyperglycemia, ketosis,acidosis, dehydration,and an electrolyteimbalance.

n The initial physicalexamination shouldfocus on hydrationstatus, central nervoussystem involvementand/or depression,and any coexistentconditions.

n The goals of therapyare to correctdehydration, restoreintravascular volume,normalize bloodglucose levels, andcorrect electrolyteand acid–baseabnormalities.

14 Vol. 22, No. 1 January 2001 Peer-Reviewed CE Article #1

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tors may include too little insulin, infection, severe stress,hypokalemia, renal failure, inadequate fluid intake, andingestion of drugs that decrease insulin secretion (e.g., β-blockers, thiazides) or cause insulin resistance (e.g., glu-cocorticoids, progestational agents).1 Many disordershave been reported to coexist with DKA,1,2 includingCushing’s syndrome, inflammatory bowel disease, pan-creatitis, pneumonia, pyoderma, pyometra, renal insuffi-ciency, and urinary tract infection.

Physical ExaminationThe initial physical examination should focus on hydra-

tion status, central nervous system involvement and/or de-pression, and any coexistent conditions. Physical findingsmay include dehydration, depression, weakness, tachycar-dia, and hypotension. Affected animals may be tachypne-ic or may experience slow, deep breathing patterns (i.e.,Kussmaul respiration). Patients may also have an acetoneodor on the breath.

Laboratory DiagnosticsLaboratory diagnostics (e.g., blood and urine glucose

levels) will be needed to confirm or support a tentative di-agnosis of DKA as well as to monitor therapy. Blood glu-cose (BG) values in dogs and cats have ranged from 200to over 1000 mg/dl (mean, 500 mg/dl).3 Ketonuria or ke-tonemia should be documented to differentiate DKA fromuncomplicated DM. Electrolyte (e.g., sodium, potassium,chloride, magnesium) and acid–base (e.g., blood gases,total CO2) disorders, which are major components of thedisease process, should also be monitored. A completeblood count, serum chemistry profile, urinalysis, andurine culture should be conducted to determine any coex-istent problems.

Nursing ManagementThe goals of therapy in DKA are to correct dehydra-

tion, restore intravascular volume, normalize BG levels,and correct electrolyte and acid–base abnormalities.

Restoring Fluid Volume DeficitThe fluid volume deficit results from decreased circu-

lating volume secondary to hyperglycemia and its induced

Diabetic Ketoacidosis Veterinary Technician January 2001 15

Figure 1—Pathophysiology of diabetic ketoacidosis.

Glossary

Chemoreceptor trigger zone—Area of the brain that results invomiting when activated; potential stimulants of this zoneinclude drugs (e.g., apomorphine, cardiac glycosides),toxins, uremia, metabolic derangements, and infections

Gluconeogenesis—Formation of glucose from noncarbohydratesources such as amino acids

Glycogenolysis—Breakdown of glycogen to glucose Glycosuria—Presence of glucose in the urine Hepatomegaly—Enlargement of the liverHyponatremia—Deficiency of sodium in the bloodIns and outs—The comparison of fluid intake (i.e., water,

intravenous fluids) versus output (i.e., urine, diarrhea,vomiting, abdominal or chest fluid)

Ketonemia—Abnormal increase of ketone bodies in thecirculating blood

Ketonuria—Presence of excess ketone bodies in the urineLipolysis—Release of free fatty acids from adipose tissuePolydipsia—Excessive or abnormal thirstPolyuria—Excessive urinationProteolysis—Splitting of proteins by hydrolysis of the peptide

bonds, with formation of smaller polypeptidesSomogyi effect—Overtreatment with insulin in diabetes

mellitus induces hypoglycemia, which in turn results inrebound hyperglycemia and ketosis

Tachypneic—Experiencing quick, shallow breathing

Insulindeficiency or resistance

Physical andmental stress

(infection/inflammation)

Decreased cellularuse of glucose

Increased glucagon/cortisol/epinephrine/growth

hormone

Hyperglycemia

Gluconeogenesis

Lipolysis

Increased ketogenesis

Ketonemia

Ketosis andmetabolic acidosis

Glycosuriaand

osmoticdiuresis

Vomiting/diarrhea;

lack of H2O

Electrolyte imbalance(sodium, potassium,

phosphate, magnesium);dehydration/hypovolemia

Decreased perfusion

Lactic acidproduction

Proteolysis

Page 3: Endocrine Emergency— Diabetic Ketoacidosis · Diabetic ketoacidosis (DKA) is a common endocrine emergency in veteri- nary medicine. DKA results in acute metabolic derangement in

osmotic diuresis. Fluid loss may also be caused by vomit-ing and lack of fluid intake. Within 20 to 24 hours afterinitiating fluid therapy, the goal is to return the patient toa normovolemic state evidenced by normal blood pres-sure; normal heart rate; normal central venous pressure;balanced ins and outs; sufficient urine production; normalskin turgor; and pink, moist mucous membranes.

A central venous catheter should be placed so that peri-odic blood samples can be easily obtained and central ve-nous pressure measurements can be taken to help guidefluid therapy. Initially, the fluid type to be administeredwill be dictated by electrolyte status. Be-cause many DKA patients also have hy-ponatremia, 0.9% saline is often given.DKA patients typically experience potassi-um depletion; therefore, fluids that are ad-ministered should be potassium enriched.Fluid rates and volumes will depend on theseverity of dehydration, the animal’s main-tenance needs, and abnormal ongoing loss-es (i.e., vomiting, diarrhea, diuresis). Cau-tion should be exercised when givinghypotonic sodium solutions because thesefluids have an increased amount of freewater relative to isotonic solutions. Toomuch free water will put the patient at riskfor developing cerebral edema. When thepatient’s glucose declines to 250 mg/dl orless, 50% dextrose should be added to thefluid therapy to make a final dextrose con-centration of 2.5% to 5%.

Normalizing Blood Glucose LevelsRegular crystalline insulin is recom-

mended for treating DKA. Insulin therapywill decrease BG levels by driving glucoseinto the cells, thereby providing them withan alternative energy source other thanketone-producing fatty acids (see Effects ofInsulin). Insulin therapy also drives po-tassium into the cells and will result indecreased serum potassium levels, thusunmasking a total body potassium deficit.Insulin protocols in-clude intermittent in-tramuscular (IM) andcontinuous low-doseintravenous (IV) infu-sion techniques.

When using the IMtechnique, insulin should

be administered hourly; the dose should be adjusted basedon the rate of declining glucose levels. Once the animal’sBG level approaches 250 mg/dl, the hourly IM insulin doseshould be administered subcutaneously every 4 to 6 hours.When the patient begins eating and drinking and is nolonger ketotic or vomiting, long-acting insulin may beused.

In the continuous low-dose IV infusion technique, theregular insulin dose should be diluted in 250 ml of 0.9%saline solution. The insulin infusion should be piggy-backed (Figure 2) onto the primary fluid line and admin-

istered with a fluid infusion pump. Be-cause insulin binds to glass and plastic, thefirst 50 ml of the infusion should be dis-carded.

Regardless of the insulin protocol used,serum glucose levels should not be al-lowed to drop too fast; otherwise, the pa-tient is at risk for developing cerebral ede-ma. Cerebral edema occurs when anosmotic gradient develops between thebrain and the extravascular fluid space.

In addition to insulin, fluid therapy canbe used to reduce serum glucose concentra-tion. Fluids enhance glucose excretion byincreasing glomerular filtration and urineflow. Fluids also decrease the secretion ofdiabetogenic hormones (i.e., epinephrine,norepinephrine, cortisol, glucagon). Dia-betogenic hormones stimulate hypergly-cemia.3

Initially, BG concentration should bemonitored every 1 to 2 hours. BG concen-tration should decline by 50 to 100 mg/dl/hour.3 Patients should be monitored forhypoglycemia, which can be characterizedby lethargy, depression, ataxia, weakness,seizures, or coma (see Insulin Overdoseand Clinical Signs of Hypoglycemia).Therapy should include IV bolus adminis-tration of 0.25 g/kg (0.5 ml/kg) of 50%dextrose followed by a continuous infusionof 2.5% to 5% dextrose.

CorrectingElectrolyte andAcid–BaseAbnormalities

As mentioned, so-dium loss through di-uresis can be correct-

16 Veterinary Technician January 2001 Diabetic Ketoacidosis

Insulin Overdose and Clinical Signs of Hypoglycemia

n Overt hypoglycemia

Lethargy, weakness,

head tilting, ataxia, seizures

n Insulin resistance

n Insulin-induced hyperglycemia

(Somogyi effect)

Effects of Insulin

n Promotes glucose uptakeby target cells

n Provides for glucosestorage

n Prevents fat and glycogenbreakdown

n Inhibits gluconeogenesisn Increases protein synthesis

Figure 2—An example of piggyback-ing fluids. In the inset, a secondary(piggybacked) line is attached to theprimary infusion line. (Copyright©

Harold Davis, BA, RVT, VTS [ECC];Davis, CA)

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Diabetic Ketoacidosis Veterinary Technician January 2001 17

ed with fluid therapy. Although the animal’s serum potas-sium concentration may initially be decreased, normal, orelevated, the patient’s total body stores of potassium mayactually be depleted. Insulin therapy will drive serumpotassium into the cells, causing a lowering of serumpotassium concentration and possibly the development ofhypokalemia. Correction of dehydration and metabolicacidosis can also cause hypokalemia by dilutional effectsand redistribution, respectively. Potassium supplementa-tion will be needed; therefore, potassium chloride shouldbe added to the fluids when serum potassium levels areknown to be low (Table I).

If potassium levels are unknown, hypokalemia may beexpected when the fluid deficit is caused by gastrointesti-nal loss, diuresis, and anorexia. Based on the magnitude of these losses, potassium de-pletion can be classified asmild, moderate, or severe;fluids should, therefore, besupplemented with 20, 30, or40 mEq/L of potassium, re-spectively. If the patient is hy-pophosphatemic, deficit re-quirements of potassium andphosphorus may be replacedby fluid supplements consist-ing of divided doses of potas-sium phosphate and potassi-um chloride. Care should beexercised when administeringpotassium supplements. Themaximum potassium adminis-tration rate is 0.5 mEq/kg/hour. Initially, electrolytesshould be monitored every 2to 4 hours. Ultimately, the pa-tient’s condition will dictatethe frequency of monitoring.

In the absence of elec-trolyte measurements, clinicalsigns and electrocardiographicmonitoring may beused. Clinical signsof hypokalemia in-clude severe muscleweakness, cervicalventroflexion, andarrhythmias. Clinicalsigns of hyperkale-mia include brady-cardia, weakness, and

neuromuscular paralysis. Subtle electrocardiographicchanges that are associated with these conditions may ap-pear (see Electrocardiographic Changes That Occur withHypokalemia and Hyperkalemia; Figure 3).

Ketones are acids that are buffered by bicarbonate in ex-tracellular fluid. When patients experience excessive ketoneproduction and bicarbonate deficits, metabolic acidosis de-velops. Decreased tissue perfusion may also contribute tothis condition. Insulin and fluid therapy will help correctacid–base abnormalities. The use of sodium bicarbonate(NaHCO3) to correct metabolic acidosis is considered con-troversial. Clear benefits of its use have not been demon-strated in humans with DKA. One study showed that NaH-CO3 may actually delay the resolution of ketosis with DKA.4 Theoretic arguments against the use of NaHCO3 in-

clude the development ofcerebral acidosis followingNaHCO3 administration.4

NaHCO3 should be consideredif the pH is less than 7.2, thebase deficit is –10 mEq/L orlarger, or the bicarbonate or–total CO2 is less than 12 mEq/L. When NaHCO3 is ad-ministered, the dosing shouldbe conservative. One option isto give enough NaHCO3 over30 minutes to correct the pHback to 7.2, base deficit to –10mEq/L, or the bicarbonate/to-tal CO2 back to 12 mEq/L.Another option is to give halfof the total base or serum bi-carbonate deficit over 6 hours.

Resolution of theDiabetic KetoacidosisAfter DKA has been re-

solved and the patient’s con-dition is stable (eating anddrinking, no vomiting), a

longer-acting insulinpreparation may beused. When the pa-tient is discharged,the owner must notifyveterinary personnelif the clinical signs ofDM (i.e., polyuria,polydipsia, polypha-gia, weight loss) or

Potassium (mEq/L)Measured Suggested

Concentration Supplementation

>5.5 03.5–5.5 53.0–3.4 202.5–2.9 302.0–2.4 40

<2.0 50

TABLE ISupplementation Guidelines

Electrocardiographic ChangesThat Occur with Hypokalemiaand Hyperkalemia

Hypokalemian Prolonged Q-T intervaln Depressed ST segmentn Depressed T-wave

amplituden Appearance of U wave

Hyperkalemian Bradycardian Decreased P-wave

amplituden Prolonged P-R intervaln Prolonged QRS complexn Spiked T wave

Figure 3—Electrocardiogram taken from a hyperkalemic (7.6 mmol/L) patient. Note theabsence of P waves, a prolonged QRS interval, and a spiked T wave. (Copyright © CraigCornell, RVT, VTS [ECC], Davis, CA)

Page 5: Endocrine Emergency— Diabetic Ketoacidosis · Diabetic ketoacidosis (DKA) is a common endocrine emergency in veteri- nary medicine. DKA results in acute metabolic derangement in

hypoglycemia (i.e., lethargy, depression, ataxia, weakness,seizures, coma) recur. Owners should be instructed tomonitor water intake, urine output, body weight, and ap-petite. When these factors are normal, diabetic patients areusually adequately controlled.5

Case Report Lulu, a 6-kg, 8-year-old spayed miniature poodle, pre-

sented with a 2-week history of vomiting that occurredtwo to three times per day forthe first week. Although thepoodle did not appear to be le-thargic, it seemed to be gettingprogressively worse. The dogbegan losing its appetite 1week earlier and becameanorectic 4 days before ad-mission. There was a historyof polyuria and polydipsia be-fore the onset of vomiting.Lulu was not on any medica-tions, and the animal’s vacci-nations were current.

On physical examination,the poodle was depressed butresponsive. Temperature was103.5°F, with a respiratoryrate of 60 breaths/minute, abody condition score of 6 outof 9, decreased skin elasticity(about 8% dehydrated), andincreased breath sounds in alllung fields. The midabdomenwas painful; large, firm in-testines were palpated withhepatomegaly present. Theright prescapular lymphnodes were enlarged at 1 to1.5 cm. The dog’s breath hadan acetone smell.

Initial PlanBased on history and physi-

cal examination findings, theveterinarian ordered a com-plete blood count to rule outinflammation and dehydra-tion. A serum chemistrypanel (including electrolytes)was conducted to assess me-tabolic and electrolyte de-

rangements (Table II). Urinalysis and culture sampleswere taken to rule out glycosuria, ketonuria, and infec-tion. An ultrasonography was obtained to assess abdomi-nal pain. A multilumen jugular catheter was placed and afluid therapy plan initiated.

Nursing Plan/GoalsWhen placing the jugular catheter, aseptic technique

was used. Steps must be taken to minimize the risk ofbacterial entry when placingor caring for indwellingcatheters. Likewise, laborato-ry samples should be ob-tained with minimal stress tothe animal. The goal of thenursing team in this case wasto develop a fluid therapyplan using lactated Ringer’ssolution assuming 8% dehy-dration (see Calculation ofLulu’s Fluid Therapy), cor-rect the dehydration over 24hours, and replace any abnor-mal fluid losses over the nextfew hours (see Nursing Ac-tions/Considerations).

Based on laboratory andimaging results, the poodle’sproblem list included DKAand pancreatitis. Serum glu-cose was 741 mg/dl, and gly-cosuria and ketonuria werepresent. In addition, Lulu hadhypokalemia, hypophospha-temia, and metabolic acido-sis. The complete blood countrevealed hemoconcentrationand leukocytosis with a leftshift and marked toxicity. Ul-trasonography of the ab-domen was compatible withpancreatitis.

Treatment andResponse

Initially, IM regular insulintherapy was initiated at 1U/hour and then decreased to0.5 U/hour. BG was mea-sured hourly; fluids were sup-plemented with dextrose to

18 Veterinary Technician January 2001 Diabetic Ketoacidosis

Reference Parameters Lulu’s Values Range

Metamyelocytes 750/µl 0Bands 9750/µl 0–300/µlLeukocytes 37,500/µl 6000–17,000/µlHematocrit 57% 37%–55%Total protein 9.6 g/dl 6.0–8.0 g/dlSerum glucose 741 mg/dl 70–120 mg/dlPotassium 2.1 mmol/L 4.1–5.3 mmol/LPhosphorus 2.9 mg/dl 3.0–6.2 mg/dlTotal carbon 11 mmol/L 16–26 mmol/L

dioxide

TABLE IILulu’s Abnormal Laboratory Values

and Reference Ranges

Nursing Actions/Considerations

n Place a jugular catheter.n Initiate a fluid therapy plan.n Monitor resolution of dehydration and restoration of

intravascular volume.n Monitor resolution of hyperglycemia and ketonuria.n Monitor and document fluid “ins and outs.”n Consider actions to be taken if pain, fluid overload,

hypoglycemia, evidence of infection, hypo- orhyperkalemia, or catheter-related problems occur.

Calculation of Lulu’s Fluid Therapy

Replacement volume (6 kg x 0.08) = 0.48 LMaintenance volume (6 kg x 75 ml/kg/day) = 0.45 LTotal volume = 0.93 L or 930 ml

930 ml ÷ 24 hours = 39 ml/hour

Note: Abnormal losses (i.e., vomiting, diarrhea, polyuria)should be made up by adding the previous hour’s abnormallosses to the next hour’s fluid input.

Page 6: Endocrine Emergency— Diabetic Ketoacidosis · Diabetic ketoacidosis (DKA) is a common endocrine emergency in veteri- nary medicine. DKA results in acute metabolic derangement in

2.5%. When the BG level approached 250 mg/dl, the vet-erinarian was consulted (see Potential Adverse Conditionsin Diabetic Ketoacidosis). The lactated Ringer’s solutionwas supplemented with 40 mEq/L potassium (split halfwith potassium chloride and half with potassium phos-phate). IV piperacillin/tazobactam sodium (168 mg) wasadministered every 6 hours. IV famotidine (3 mg) was giv-en every 24 hours. Serum electrolytes and venous bloodgases were monitored every 4 hours. The poodle was giv-en nothing by mouth. Temperature, pulse, and respirationwere checked every 4 hours (for the first 24 hours) andthen every 6 hours. IM oxymorphone (0.05 mg/kg) wasadministered every 4 hours as needed for pain.

Lulu’s glucose reached 220 mg/dl within 12 hours, andthe ketonuria was resolved. With regard to the fluid thera-py, 50% dextrose was added to make a 2.5% solution.The patient was started on NPH insulin. At the time ofdischarge (the sixth hospital day), Lulu was regulated onNPH insulin twice daily.

SummaryDiabetic ketoacidosis is a complex endocrine/metabolic

disorder. After animals are diagnosed with DKA, a thera-peutic plan should be implemented and the patient’s re-sponse to therapy monitored.

An IV catheter should be placed and fluids should beadministered as directed by the veterinarian. Techniciansmust be capable of monitoring vital signs as well as theresolution of hypovolemia and dehydration and must also

be able to recognize the signs of fluid overload and prob-lems associated with catheterization. Insulin therapy mustbe properly administered. Technicians, therefore, must beaware of potential side effects as well as recognize thesigns of insulin overdose.

Finally, technicians should be able to monitor the cor-rection of acid–base and electrolyte abnormalities eitherthrough blood sample analysis or by assessing clinicalsigns and monitoring electrocardiographic readings. Insummary, technicians must be able to recognize adversesituations as well as know how to treat them. A collabora-tive team effort gives patients the best chance of recovery.

References1. Nichols R, Crenshaw KL: Complications and concurrent disease

associated with diabetic ketoacidosis and other severe forms ofdiabetes mellitus, in Greco DS, Peterson ME (eds): VeterinaryClinics of North America Small Animal Practice: Diabetes Mel-litus. Philadelphia, WB Saunders Co, 1995, pp 617–624.

2. Schaer M: Metabolic emergencies: Diabetic ketoacidosis. KalKan Waltham Symp Treat Small Anim Dis Emerg Crit CareProc:61–67, 1991.

3. Feldman EC, Nelson RW: Diabetic ketoacidosis, in Canineand Feline Endocrinology and Reproduction. Philadelphia,WB Saunders Co, 1996, pp 392–421.

4. DiBartola SP: Metabolic acid–base disorders, in DiBartola SP(ed): Fluid Therapy in Small Animal Practice. Philadelphia,WB Saunders Co, 2000, p 221.

5. Nelson RW: Disorders of the endocrine pancreas, in NelsonRW, Couto CG (eds): Small Animal Internal Medicine. St.Louis, Mosby, 1998, p 759.

About the AuthorMr. Davis is affiliated with the Emergency NursingService, Veterinary Medical Teaching Hospital, Uni-versity of California, Davis, and is co-founder of theAcademy of Veterinary Emergency and Critical CareTechnicians. He has extensive experience in the fieldof emergency and critical care medicine.

1. ___________ is not characteristic of DKA.a. Ketosisb. Alkalosisc. Dehydrationd. Hyperglycemia

20 Veterinary Technician January 2001 Diabetic Ketoacidosis

Potential Adverse Conditionsin Diabetic Ketoacidosis

A veterinarian should be consulted if the patient experiences:n A heart rate <60 or >160 beats/minn Systolic blood pressure <80 mm Hg or decrease ≥20 mm

Hg from baselinen Mean blood pressure <60 mm Hg or decrease ≥10 mm Hg

from baselinen Central venous pressure <0 cm H2O or decrease 3 cm H2O

from baseline n Urine output <1 ml/kg/hour for 2 consecutive hoursn Signs consistent with fluid overloadn Blood glucose <250 mg/dl or decrease in blood glucose

>100 mg/dl/hourn Altered consciousness levelsn Arrhythmias or electrocardiographic changes consistent

with hyperkalemian Electrolyte and acid–base abnormalitiesn Evidence of infection

The article you have read is the equivalent of 1⁄2 hour of study. Toreceive credit for your study, choose only the one best answer to

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2. _____________ occurs when hyperglycemia exceeds therenal threshold. a. Potassium resorptionb. Sodium resorptionc. Osmotic diuresisd. Water retention

3. Which of the following is a potential risk factor for DKA?a. too little insulinb. increased insulin secretionc. increased ketone metabolismd. a high-fiber diet

4. ____________ has been reported to coexist with DKA.a. Respiratory distress syndromeb. A portosystemic shuntc. Glaucomad. Cushing’s syndrome

5. Which of the following is not a goal of DKA therapy?a. reduction of total CO2

b. correction of dehydrationc. normalization of BG leveld. correction of serum electrolyte abnormalities

6. Which type of fluid places diabetic patients at risk forcerebral edema?a. plasma c. hypotonicb. isotonic d. whole blood

7. Insulin administration a. increases serum glucose.b. drives potassium into the cells.c. drives potassium out of the cells.d. increases ketone production.

8. Glucose reduction should not exceed ________ mg/dl/hour.a. 25b. 50c. 75d. 100

9. What is the likely cause if the following electrocardio-graphic changes occur: bradycardia, decreased P-waveamplitude, prolonged P-R interval and QRS complex,and spiked T wave?a. hypokalemiab. hyperkalemiac. hypercalcemiad. hypocalcemia

10. Which acid–base disturbance does NaHCO3 correct?a. respiratory alkalosisb. respiratory acidosisc. metabolic acidosisd. metabolic alkalosis

Veterinary Technician January 2001 21