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Clinical pearls, article information, case study: diabetic ketoacidosis in type 2 diabetes: “look under the sheets”.

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Brian J. Welch , Ivana Zib; Case Study: Diabetic Ketoacidosis in Type 2 Diabetes: “Look Under the Sheets”. Clin Diabetes 1 October 2004; 22 (4): 198–200. https://doi.org/10.2337/diaclin.22.4.198

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Diabetic ketoacidosis (DKA) is a cardinal feature of type 1 diabetes. However, there is a strong, almost dogmatic, errant perception by physicians that DKA is a complication that only occurs in patients with type 1 diabetes. This is not true. DKA does occur in type 2 diabetes; however, it rarely occurs in the absence of a precipitating event.

R.T., a 25-year-old African-American man with type 2 diabetes presented with a 5-day history of nausea and vomiting. He also reported a 2-week history of polyuria and polydipsia and a 10-lb weight loss. A review of symptoms was pertinent for a 5-day history of persistent lower back pain.

The patient was diagnosed with type 2 diabetes 5 years ago when he presented to a different hospital with symptoms of polyuria, polydipsia, and weight loss. He was given a prescription for a sulfonylurea, which he says he took until his initial prescription ran out 1 month later. He had not taken any other medication since that time.

Physical examination revealed an afebrile, obese man (BMI 40 kg/m 2 ) with prominent acanthosis nigricans, no retinopathy by direct funduscopic exam, and a normal neurological exam, including motor function and sensation. The patient had no tenderness to palpation over the lumbrosacral spine or paraspinous muscles despite his complaint of lower back pain.

The laboratory data showed an anion gap, metabolic acidosis, and hyperglycemia (pH of 7.14, anion gap of 24, bicarbonate 6 mmol/l, urinary ketones 150 mg/dl, glucose 314 mg/dl) consistent with the diagnosis of DKA. His white blood count was 20,400/μl. Urinalysis demonstrated no evidence of infection. The patient's hemoglobin A 1c (A1C) was 13.5%.

The patient was admitted and treated aggressively with intravenous fluid and an insulin-glucose infusion. A non-contrast magnetic resonance imaging(MRI) of the lumbosacral spine (L-spine) was obtained because of the patient's persistent complaint of lower back pain. The L-spine MRI results were negative for pathology. However, R.T. reported increasing discomfort and now noted weakness and numbness in his bilateral lower extremities.

Neurology was consulted, and during their assessment, the patient became incontinent and was found to have 0/5 strength in the lower extremities,severely compromised sensation, and decreased rectal tone. A contrast MRI of both the thoracic and lumbar spine was ordered, and the patient was found to have a T10-T12 epidural abscess ( Figure 1 ).

Epidural abscess precipitating DKA in a type 2 diabetic patient.

The patient's antibiotic coverage was broadly expanded, high-dose intravenous steroids were initiated, and neurosurgery was urgently consulted. Emergent evacuation of the epidural abscess with laminectomies of T10-T12 was performed without complication.

R.T.'s neurogenic bladder resolved without further intervention. After intensive inpatient rehabilitation, he had 3/5 strength in bilateral lower extremities and was still unable to ambulate.

S.D., a 39-year-old white man with type 2 diabetes and mild mental retardation, presented with a 3-week history of polyuria and polydipsia, as well as dysuria, left hip pain, and a feeling of incomplete bladder emptying. Because of the severity of his left hip discomfort, the patient required a cane to ambulate.

The patient was diagnosed with type 2 diabetes 4 years ago on the basis of an elevated fasting blood glucose level during a routine medical examination. He was started on oral hypoglycemic agents, but he discontinued them after 1 month because he was unable to pay for them.

On physical exam, S.D. was afebrile but tachycardic (heart rate 131 bpm)and hypertensive (blood pressure 192/118 mmHg). General examination revealed a wasted, severely volume-depleted man. Thrush was observed on oropharyngeal exam. Cardiopulmonary and abdominal examinations were unremarkable. The patient had point tenderness on the anterior aspect of his left hip. Rectal examination revealed a non-tender prostate.

The laboratory data showed an anion gap, metabolic acidosis, and hyperglycemia (pH 7.24, bicarbonate 9 mmol/l, anion gap 24, urinary ketones 150 mg/dl, and glucose 322 mg/dl) consistent with the diagnosis of DKA. Urinalysis was remarkable for large blood, 4+ bacteria, and > 400 white blood cells. S.D.'s serum white blood count was 22,200, and his erythrocyte sedimentation rate was 109 mm/hour. His A1C result was 12.6%.

The patient was admitted and treated with intravenous fluids and an insulin-glucose infusion. Cultures were obtained. S.D. was started empirically on ticarcillin/clavulanic acid because of concern for left hip osteomyelitis and complicated urinary tract infection. An MRI of the left hip was ordered to evaluate for suspected osteomyelitis. Unexpectedly, it revealed left hip myonecrosis and a large loculated prostatic abscess( Figure 2 ).

Prostatic abscess precipitating DKA in a type 2 diabetic patient.

Urology was consulted, and the patient underwent transurethral drainage of the prostatic abscess. Methicillin-sensitive Staphylococcus aureus grew from both blood and urine cultures. S.D. was treated with intravenous antibiotics per culture sensitivities. The myonecrosis was treated conservatively.

The patient recovered well. He was started on subcutaneous insulin and discharged home to complete a 2-week course of intravenous antibiotics.

What is the mechanism of DKA?

Why does DKA occur in type 2 diabetes?

DKA is a cardinal feature of type 1 diabetes, which has led to the widespread errant perception that it is a complication unique to type 1 diabetes. However, it has been repeatedly reported that DKA does occur in patients with type 2 diabetes. 1 - 5   Moreover, as the cases presented here illustrate, it can occur even in patients who were previously insulinindependent.

A recent study evaluating 138 consecutive admissions for DKA at a large academic center observed that 21.7% had type 2 diabetes. 6   Nearly 70% of the admissions involved discontinuation of medications, and almost half had an identifiable infection when an intensive search was undertaken.

A review of the mechanism of DKA is important. Ketoacidosis occurs as a function not only of severe insulin deficiency, but also of elevated glucagon levels. Insulin is an anabolic hormone. Severe insulin deficiency results in decreased glucose utilization by muscle and an unregulated increase in lipolysis. This leads to an enhanced delivery of gluconeogenetic precursors(glycerol and alanine) to the liver. Furthermore, removal of the normal suppressive effect of insulin causes glucagon elevation. 7 , 8   Glucagon is a catabolic hormone. Glucagon promotes gluconeogenesis, decreases oxidation of free fatty acids to triglycerides, and promotes hepatic ketogenesis. 9  

Importantly, the concentration of insulin required to suppress lipolysis is only one-tenth of that required to promote glucose utilization. 10   Typically, moderate insulin deficiency (as observed in patients with type 2 diabetes) is associated with sufficient insulin to block lipolysis (and therefore ketoacid formation), but not enough to promote glucose utilization. This leads to hyperglycemia without formation of the ketoacids.

When DKA occurs in patients with type 2 diabetes, the presumed mechanism of ketoacidosis is the combination of relative insulin deficiency and increased secretion of glucagon (as well as other counteregulatory hormones such as cortisol, catecholamines, and growth hormone) in response to stress from 1 ) overwhelming infection, 2 ) infarction of tissue, or 3 ) other severe illness. The elevated catecholamines further suppress insulin secretion to perpetuate a downward spiral. The increased glucagons-to-insulin ratio causes a mismatch that promotes unregulated lipolysis and proteolysis with subsequent uninterrupted formation of ketoacids.

To summarize, DKA is not a unique feature of type 1 diabetes. Though much more common in type 1 diabetes, it does occur in patients with type 2 diabetes, as illustrated by these case reports. However, it is rare for DKA to occur in type 2 diabetes in the absence of some precipitating event. When DKA occurs in an individual with type 2 diabetes, the clinician should “look under the sheets” and initiate an intensive search for the precipitating factor. Once identified, the trigger should be treated promptly and appropriately.

DKA does occur in type 2 diabetes.

DKA in type 2 diabetes rarely occurs without a trigger.

When it does, an intensive search for the precipitating factor should be undertaken.

Brian J. Welch, MD, and Ivana Zib, MD, are fellows in the Division of Endocrinology and Metabolism at the University of Texas Southwestern Medical Center in Dallas.

The authors thank Philip Raskin, MD, for his support and guidance.

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DIABETIC KETOACIDOSIS PROTOCOL

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Diabetic Ketoacidosis Management - PowerPoint PPT Presentation

Diabetic Ketoacidosis Management

Diabetic ketoacidosis management heidi chamberlain shea, md endocrine associates of dallas goals of discussion pathophysiology of dka biochemical criteria for dka ... – powerpoint ppt presentation.

• Heidi Chamberlain Shea, MD
• Endocrine Associates of Dallas
• Pathophysiology of DKA
• Biochemical criteria for DKA
• Treatment of DKA
• Prevention of DKA
• Hyperosmolar Nonketoic Syndrome
• Annual incidence in U.S.
• 5-8 per 1000 diabetic subjects
• 2.8 of all diabetic admissions are due to DKA
• Overall mortality rate ranges from 2-10
• Higher is older patients
• Failure to take insulin
• Failure to increase insulin
• Illness/Infection
• Acute stress
• Medical Stress
• Counterregulatory hormones
• Oppose insulin
• Stimulate glucagon release
• Hypovolmemia
• Increases glucagon and catecholamines
• Decreased renal blood flow
• Decreases glucagon degradation by the kidney
• Severe insulin deficiency
• Excess counterregulatory hormones
• Epinephrine
• Growth hormone
• Required for transport of glucose into
• Inhibits lipolysis
• Absence of insulin
• Glucose accumulates in the blood
• Uses amino acids for gluconeogenesis
• Converts fatty acids into ketone bodies
• Acetone, Acetoacetate, ß-hydroxybutyrate
• Increased counterregulatory hormones
• Polyuria, polydipsia
• Dehydration
• Tachycardia
• Orthostasis
• Abdominal pain
• Fruity breath
• Kussmaul breathing
• Mental status changes
• Hyperglycemia
• Anion gap acidosis
• (Na K) (Cl Bicarb) gt12
• Bicarbonate lt15 mEq/L
• Urine ketones and serum ketones
• Hyperosmolarity
• Alcoholic ketoacidosis
• Lactic acidosis
• Renal failure
• Ethylene glycol or methyl alcohol poisoning
• Starvation in late pregnancy or lactation (rare)
• DKA can be present with BS lt300
• Impaired gluconeogenesis
• Liver disease
• Acute alcohol ingestion
• Prolonged fasting
• Insulin-independent glucose is high (pregnancy)
• Chronic poor control but taking insulin
• Bedside urine ketones false negatives
• Measure acetoacetate not ß-hydroxybutyrate
• Send blood to lab
• Initial hospital management
• Replace fluid and electrolytes
• IV Insulin therapy
• Glucose administration
• Watch for complications
• Disconnect insulin pump
• Once resolved
• Convert to home insulin regimen
• Prevent recurrence
• Fluid replacement
• Restores perfusion of the tissues
• Lowers counterregulatory hormones
• Average fluid deficit 3-5 liters
• Initial resuscitation
• 1-2 liters of normal saline over the first 2 hours
• Slower rates of 500cc/hr x 4 hrs or 250 cc/hr x 4 hours
• When fluid overload is a concern
• If hypernatremia develops ½ NS can be used
• Hyperkalemia initially present
• Resolves quickly with insulin drip
• Once urine output is present and Klt5.0, add 20-40 meq KCL per liter.
• Normo/Hypokalemia
• Malnourished individuals (alcoholics)
• Start K replacement and have K gt 3.0 prior to start of insulin
• Remember to check Magnesium
• Phosphate deficit
• May want to use Kphos
• Bicarbonate not given unless pH lt7 or bicarbonate lt5 mmol/L
• IV bolus of 0.1-0.2 units/kg ( 10 units) regular insulin
• Follow with hourly regular insulin infusion
• Glucose levels
• Decrease 75-100 mg/dl hour
• Minimize rapid fluid shifts
• Continue IV insulin until urine is free of ketones
• Supplemental glucose
• Hypoglycemia occurs
• Insulin has restored glucose uptake
• Suppressed glucagon
• Prevents rapid decline in plasma osmolality
• Rapid decrease in insulin could lead to cerebral edema
• Glucose decreases before ketone levels decrease
• Start glucose when plasma glucose lt300 mg/dl
• Precipitates DKA
• Leukocytosis can be secondary to acidosis
• If not improving with fluids r/o MI
• Vascular thrombosis
• Severe dehydration
• Cerebral vessels
• Occurs hours to days after DKA
• Pulmonary Edema
• Result of aggressive fluid resuscitation
• Cerebral Edema
• First 24 hours
• Tx Mannitol
• May require intubation with hyperventilation
• Most patients require 0.5-0.6 units/kg/day
• Pubertal or highly insulin resistant patients
• 0.8-1.0 units/kg/day
• Long acting insulin
• 1/2-2/3 daily requirement
• NPH, Levemir or Lantus
• Short acting insulin
• 1/3-1/2 given at meals
• Regular, Humalog, Novolog or Apidra
• Give SQ insulin at least 2 hours prior to stopping insulin infusion.
• Lantus or Levemir
• Steady state at 2-4 hrs
• Short acting analogs for meal times
• If transitioning to the pump
• Restart the pump and after 30 minutes stop insulin infusion
• May still be more insulin resistant so will need more than usual dose
• Check blood sugars in 2 hrs
• Offer supplemental
• Never omit insulin
• Cut long acting in half
• Prevent dehydration and hypoglycemia
• Monitor blood sugars frequently
• Monitor for ketosis
• Provide supplemental fast acting insulin
• Treat underlying triggers
• Maintain contact with medical team
• Do not stop insulin but adjust
• If gt 300 mg/dl, then check urine ketones
• If ketones positive
• Increase fluids
• Take supplemental insulin Q2 hrs
• Insulin temperature sensitive
• lt 77 degrees
• Teenagers, homeless, pen and pump users
• Do not store insulin in the car
• Traveling and summer outdoor activities
• May need to replace more frequently
• Extreme hyperglycemia and dehydration
• Unable to excrete glucose as quickly as it enters the extracellular space
• Maximum hepatic glucose output results in a plateau of plasma glucose no higher than 300-500 mg/dl
• When sum of glucose excretion plus metabolism is less than the rate which glucose enters extracellular space.
• Extreme hyperglycemia and hyperosmolarity
• High mortality (12-46)
• Older patients with intercurrent illness
• Impaired ability to ingest fluids
• Urine volume falls
• Decreased glucose excretion
• Elevated glucose causes CNS dysfunction and fluid intake impaired
• Some insulin may be present
• Extreme hyperglycemia inhibits lipolysis
• Extreme dehydration
• Supine or orthostatic hypotension
• Confusion coma
• Neurological findings
• Transient hemiparesis
• Hyperreflexia
• Generalized areflexia
• Glucose gt600 mg/dl
• Normal, elevated or low
• Normal or elevated
• Bicarbonate gt15 mEq/L
• Osmolality gt320 mOsm/L
• Fluid repletion
• NS 2-3 liters rapidly
• Total deficit 10 liters
• Replete ½ in first 6 hours
• Make sure perfusion is adequate
• Insulin drip 0.1U/kg/hr
• Treat underlying precipitating illness
• Fluid shift and shock
• Giving insulin without sufficient fluids
• Using hypertonic glucose solutions
• Hyperkalemia
• Premature potassium administration before insulin has begun to act
• Hypokalemia
• Failure to administer potassium once levels falling
• Recurrent ketoacidosis
• Premature discontinuation of insulin and fluids when ketones still present
• Hypoglycemia
• Insufficient glucose administration
• Successful management requires
• Judicious use of fluids
• Establish good perfusion
• Insulin drip
• Steady decline
• Complete resolution of ketosis
• Electrolyte replacement
• Frequent neurological evaluations
• High suspicion for complications
• Determine etiology to avoid recurrent episodes

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Diabetic ketoacidosis

• Overview  
• Theory  
• Diagnosis  
• Management  
• Follow up  
• Resources  

Case history

A 20-year-old man is brought to the emergency department with abdominal pain, nausea, and vomiting with increasing polyuria, polydipsia, and drowsiness since the day before. He was diagnosed with type 1 diabetes 2 years previously. He mentions that he ran out of insulin 2 days ago. Vital signs at admission are: BP 106/67 mmHg, heart rate 123 beats per minute, respiratory rate 32 breaths per minute, temperature 98.8°F (37.1°C). On mental status examination, he is drowsy. Physical examination reveals Kussmaul breathing (deep and rapid respiration due to ketoacidosis) with acetone odor and mild generalized abdominal tenderness without guarding and rebound tenderness. Initial laboratory data are: blood glucose 450 mg/dL, arterial pH 7.24, pCO₂ 25 mmHg, bicarbonate 12 mEq/L, WBC count 18,500/microliter, sodium 128 mEq/L, potassium 5.2 mEq/L, chloride 97 mEq/L, BUN 32 mg/dL, creatinine 1.7 mg/dL, serum ketones strongly positive.

Other presentations

It is now well recognized that new-onset type 2 diabetes can manifest with DKA. These patients are obese and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin resistance. However, after treatment of the acute hyperglycemic episode with insulin, beta-cell function and insulin effects improve so these patients are able to discontinue insulin therapy and may be treated orally or by diet alone, with 40% remaining insulin-independent 10 years following the initial episodes of DKA. These patients do not have the typical autoimmune laboratory findings of type 1 diabetes. [2] Balasubramanyam A, Nalini R, Hampe CS, et al. Syndromes of ketosis-prone diabetes mellitus. Endocr Rev. 2008 May;29(3):292-302. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2528854 http://www.ncbi.nlm.nih.gov/pubmed/18292467?tool=bestpractice.com This type of diabetes has been labeled as "type 1 and ½" or "type 1 and a half" diabetes, "Flatbush" diabetes, or "ketosis-prone" diabetes. Conversely, an extreme hyperosmolar state similar to hyperosmolar hyperglycemic state (HHS) has been reported in combination with DKA in type 1 diabetes. [3] Umpierrez GE, Woo W, Hagopian WA, et al. Immunogenetic analysis suggests different pathogenesis for obese and lean African-Americans with diabetic ketoacidosis. Diabetes Care. 1999 Sep;22(9):1517-23. http://www.ncbi.nlm.nih.gov/pubmed/10480519?tool=bestpractice.com [4] Mauvais-Jarvis F, Sobngwi E, Porcher R, et al. Ketosis-prone type 2 diabetes in patients of sub-Saharan African origin: clinical pathophysiology and natural history of beta-cell dysfunction and insulin resistance. Diabetes. 2004 Mar;53(3):645-53. https://diabetes.diabetesjournals.org/content/53/3/645.full http://www.ncbi.nlm.nih.gov/pubmed/14988248?tool=bestpractice.com [5] Umpierrez GE, Smiley D, Kitabchi AE. Narrative review: ketosis-prone type 2 diabetes mellitus. Ann Intern Med. 2006 Mar 7;144(5):350-7. http://www.ncbi.nlm.nih.gov/pubmed/16520476?tool=bestpractice.com [6] Kitabchi AE, Umpierrez GE, Fisher JN, et al. Thirty years of personal experience in hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state. J Clin Endocrinol Metab. 2008 May;93(5):1541-52. http://www.ncbi.nlm.nih.gov/pubmed/18270259?tool=bestpractice.com

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A CASE PRESENTATION OF A PATIENT WITH DIABETIC KETOACIDOCIS (DKA)

Aug 22, 2014

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A CASE PRESENTATION OF A PATIENT WITH DIABETIC KETOACIDOCIS (DKA). Prepared by: Tristan Villanueva Arcibal BSN-RN Presented on: July 16, 2013. DEMOGRAPHIC DATA. Name : Mr. X Case no . :201--- Age : 28 y/o Gender : Male Nationality : Saudi Admission date : 11-4-2013

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A CASE PRESENTATION OF A PATIENT WITH DIABETIC KETOACIDOCIS (DKA) Prepared by: Tristan Villanueva Arcibal BSN-RN Presented on: July 16, 2013

DEMOGRAPHIC DATA • Name: Mr. X • Case no. :201--- • Age: 28 y/o • Gender: Male • Nationality: Saudi • Admission date: 11-4-2013 • Time of arrival: 0840H • Chief complaints: Persistent vomiting,Low blood pressure, High blood glucose, Altered mental status • Diagnosis: DKA

PHYSICAL ASSESSMENT • HEAD • Altered mental status ( restless and agitation) • GCS 12/15 • Eye response (3) : Responds to verbal command • Verbal response (4) : Confused • Motor response (5): Localizes pain • EYES • Pupils • Reactive to light • Round and equal in size

ENT • Dry oral mucosa • (+) Ketotic/ acetone breath • CHEST • Rapid breathing (30 cycles per minute) • Equal breath sounds • Symmetrical chest rise • No adventitious sounds (ex: wheezing, crackles) • HEART • Regular but rapid HR: 110 BPM • BP: 90/60 mmhg • S2> S1

ABDOMEN • (+) nausea and vomiting • Soft and non tender abdomen • Bowel sounds (+) • No signs of rebound tenderness, trauma & abdominal distention • GUT • Excessive urination • SKIN • Poor skin turgor

EXTREMITIES • Limbs are normal • (-) weakness, contractures, joint swelling/ paralysis

PAST MEDICAL HISTORY • Patient has Type 1 Diabetes Mellitus/ IDDM since 15 years with maintenance medication of Regular Insulin twice daily via subcutaneous route before meals.

SLIDING SCALE

PRESENT MEDICAL HISTORY • Patient was conveyed by Red Crescent Authority and was allegedly found unconscious inside his car. • Upon arrival to ER, patient was persistently vomiting, restless and disoriented . • Vital signs: BP 90/60 mmHG, PR 110 BPM, RR 30, Temp. 36.8 ,SPO2 98%, Blood Glucose 450 mg/dl. • Prior to confinement patient consumed large amount of alcohol and had failed to comply with his medication regimen.

Laboratory tests: • Glucose (random): 23.4 mmo/L (3.9-7.8 mmo/L) • Urinalysis : ++ketones • CBC • WBC: 9.04 (4.23-9.07) • HGB: 14.3 (13.7-17.5) • HCT: 39.6 (40.1-51.0) • PLT: 350 (163-337) • Electrolytes: • NA+: 141 mmO/L (135-150 mmO/L) • K+:4.3 mmO/L ( 3.5- 5.0 mmO/L) • Cl+ :98 mmO/L (98-111 mmO/L) • BUN: 4.42 mmO/L (1.8-8.3 mmO/L) • Creatinine: 75.98 (58-110)

ECG tracing: • Rate: 110 BPM • Presence of P wave • PR interval: <0. 20 secs. • QRS: <0.12 secs. • ABG result: • Ph: 7.33 (7.35-7.45) • PCO2: 34.5 mmHG ( 35-45 mmHG) • HC03: 20. 2 mEq/L (22-26 mEq/L

DIABETICKETOACIDOSIS • Diabetic ketoacidosis, or DKA, is a serious and possibly life-threatening condition that results from not having enough insulin characterized by hyperglycemia,ketonuria, acidocis and dehydration. • DKA is a medical emergency, and without treatment it can lead to death. DKA was first described in 1886; until the introduction of insulin therapy in the 1920s and was almost universally fatal.

DKA is most likely to occur in the early stage of type 1 diabetes before a diagnosis is made, during periods of sickness or when too little insulin is taken

ANATOMY AND PHYSIOLOGY OF THE PANCREAS

The pancreas is about 6 inches long and sits across the back of the abdomen, behind the stomach. The head of the pancreas is on the right side of the abdomen and is connected to the duodenum (the first section of the small intestine) through a small tube called the pancreatic duct. The narrow end of the pancreas, called the tail, extends to the left side of the body. • The pancreas is a dual-function gland, having features of both endocrine and exocrine glands.

The part of the pancreas with endocrine function is made up of approximately a million] cell clusters called Islets of Langerhans. Four main cell types exist in the islets • α cells: secrete glucagon (increase glucose in blood), • β cells: secrete insulin (decrease glucose in blood), • Delta cells: secrete somatostatin (regulates/stops α and β cells), • Gamma cells:secrete pancreatic polypeptide. • The pancreas as an exocrine gland helps out the digestive system. It secretes pancreatic fluid that contains digestive enzymes that pass to the small intestine. These enzymes help to further break down the carbohydrates, proteins, and lipids (fats) in the chyme.

PATHOPHYSIOLOGY OF DKA

Decreased or absent insulin production Decreased or absent insulin production Increased blood glucose (Hyperglycemia) Fat metabolism • Osmotic Diuresis • Polyuria • Polydipsia • ketonuria Ketone bodies (Metabolic acidosis) Dehydration and electrolyte imbalance eg. hypotension • Compensatory Respiratory alkalosis) DKA

In various situations such as infection, insulin demands rise but are not matched by the failing pancreas. Blood sugars rise, dehydration ensues, and resistance to the normal effects of insulin increases further by way of a vicious circle. • Osmotic diuresis caused by hyperglycemia creates a shift in electrolytes with losses in potassium, sodium, phosphate and water.

ETIOLOGY • DKA most frequently occurs in those who already have diabetes, but it may also be the first presentation in someone who had not previously been known to be diabetic. • intercurrent illness (pneumonia, influenza, gastroenteritis, a urinary tract infection) •  pregnancy, inadequate insulin administration •  myocardial infarction (heart attack), stroke

Young patients with underlying eating disorder/ starvation, or may be using insufficient insulin for fear that it will cause weight gain. • Obesity, strong family history • Excessive alcohol intake/ use of cocaine • African, African-American and Hispanic people.

CLINICAL MANIFESTATIONS The symptoms of an episode of diabetic ketoacidosis usually evolve over the period of about 24 hours. • Nausea and vomiting • Excessive thirst. • Excessive urination • Abdominal pain that may be severe • Hyperglycemia

tachycardic (a fast heart rate) and low blood pressure may be observed. • "ketotic" odor is present, which is often described as "fruity", often compared to the smell of pear drops whose scent is a ketone. • Hyperventilation/ Kussmauls respiration • Fatigue

INTERVENTIONS/ TREATMENTS • Oxygen administration via non-rebreathing mask at 7 LPM. • Obtaining Vital Signs and blood sugar level. • Establishing peripheral IV access. • Obtaining Blood samples for laboratory investigations. • ABG sampling. • Fluid replacement (IVF NSS 1L).

Humulin R 10 units IV. • Obtaining ECG and Chest Xray. • Regular Insulin infusion ( IVF NSS 60 ML + Regular insulin 24 units at 15 ml/hr) • Premosan 10 MG IV. • Foleys catheterization. • Blood Glucose monitoring.

Implemented safety precautions (e.g. Siderails elevated). • Admission to Intensive care for close monitoring.

COMPLICATIONS • Cerebral edema • Low potassium (hypokalemia) • Hypovolemia • Death can occur without prompt management.

PHARMACOLOGY • Insulin is a peptide hormone, produced by beta cells of the pancreas, and is important for the utilization of glucose for cellular metabolism as well as proper metabolism of protein and fat.

TYPES OF INSULIN

SIDE EFFECTS OF INSULIN • Blurry vision. • Disturbed sensations. • Hypoglycemia • Allergic reaction. It can be moderate or even severe. Moderate symptoms include swelling, itchy or squeezing at injection place. Severe symptoms among other are: pulse become quickly, blood pressure descends, squeezing all over the body, breath become difficult. If a patient experiences the severe symptoms, he/she should immediately contact his/her doctor. ..

Lipodystrophy is a medical condition characterized by abnormal or degenerative conditions of the body's adipose tissue. ("Lipo" is Greek for "fat" and "dystrophy" is Greek for "abnormal or degenerative condition".) A more specific term, lipoatrophy is used when describing the loss of fat from one area.

PRIORITIZATION OF NURSING PROBLEMS • Fluid Volume deficit and Risk for Electrolyte imbalance • Impaired Breathing pattern • Risk for fall secondary to impaired neurologic function • Imbalanced Nutrition

NURSING CARE PLAN

NURSING HEALTH TEACHING • Never omit insulin dosage. Take the usual dosage of insulin as prescribed. Compliance of medication regimen is significant. • Monitor blood glucose every 2-4 hours. Record test results. • Drink plenty of fluids 6-8 oz of water every hour is recommended. • If unable to eat, drink fluids that contain carbohydrates such as fruit juices, regular soda. • Seek health care provider if illness becomes severe or unmanageable

Rotate injection sites for insulin administration to prevent muscle atrophy. • Inspect the feet carefully and daily for calluses, corns, blisters, abrasions, redness and nail abnormalities • Prevent moisture between toes to prevent maceration of the skin. • Wear well fitting non compressive shoes.

CONCLUSION It is to significant to determine DKA as early as possible for emergent intervention. DKA is a life threatening condition but with early detection the better the prognosis. Nurses play a vital role in managing or preventing DKA. Patients who are at risk for developing DKA can also do their part by complying with their medication regimen, avoiding alcohol, and knowing the manifestations that need prompt treatment. Managing DKA is a multidisciplinary approach from Physician, Nurses and other healthcare staff.

REFERENCES • http://en.wikipedia.org/wiki/Diabetic_ketoacidosis • Mosby’s Comprehensive Review of NCLEX-RN Examination 19th Edition • Saunder’s NCLEX-RN review 9th Edition • Lippincott Manual of Nursing Practice 9th Edition

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