Case Study
Content
J G COLLEGE OF NURSING AHMEDABAD SUBJECT:ADVANCE NURSING PRACTICE
TOPIC:case study
SUBMITTED TO PROF.MR.YONATAN LECTURER J G COLLEGE OF NURSING SUBMITTED BY BINAL JOSHI F Y MSC NURSING J G COLLEGE OF NURSING
PATIENT’S BIODATA: NAME AGE SEX : Mr. prakash shah : 33years : male : Dr. Biren Hashvadan
DOCTOR’S UNIT
DATE OF ADMISSION : 8 /11/2010 REGISTRATION NO ADDRESS : 68099 : 45,bandhan society Sarkhej, Ahmedabad- 380082 MOBILE NO MARITAL STATUS OCCUPATION RELIGION NATIONALITY DIAGNOSIS : 9567244120 : Married : company worker : Hindu : Indian : congestive heart failure HISTORY OF PATIENT: CHIEF COMPLAINS: Mr. vanaraj was admitted in medical intensive care unit of shalby hospital with the complaints of vomiting since 2 days and abdominal pain since 1 day, history of altered consciousness since today morning,, fever is also present. At the time of admission vital signs. Respiration – gasping respiration. Pulse – feasible pulse present. Temperature- 100F. Blood pressure- 80/ 40 mm of hg. Emergency treatment given to the patient that is endotrachel intubation done and ventilator support given by AMBU bag.
PRESENT HISTORY Today patient is unconscious, not oriented to time, place and person, now also he is on ventilator support .Central venous catheter is inserted using triple lumen catheter into internal jugular vein ,iv fluids RL is going on. Chest leads applied on chest and attach with cardiac monitoring. Cardiac monitoring is continuing. Today 1 episodes of vomiting in morning and nausea also present. Blood pressure is decreased 80/40. So inj dopamine is going on via infusion pump. Urinary catheter is present, urine output is 1800ml /day. His temperature sometimes get high, it was 101 F, So antipyretic injection febrinil was given to him, Vital signs • • • • • Respiration Pulse Temperature :14breaths/min : 68beats/min :100 F
Blood pressure: 100/50 mm of hg RBS : 410mg/dl
PAST HISTORY: Mr.vanaraj has past history of diabetes mellitus since 10 years he is taking tab metformin 10 mg . no any other medical illness. He has no any surgical past history. Before 5 years he had jaundice ,and before 3 years he had falisparum malaria also for that he had 2 times hospitalize for treatment. He had complains had breathlessness along with chronic coughing, also he had suffered from chronic constipation for that he was taking some ayurvedic tablets as per advised by ayurvedic doctor.
PERSONAL HISTORY: Mr.vanaraj ,he was admitted in Medical ICU on 8th November,2010 ;he is working in company .His wife is housewife. He has two children one boy and one girl. He is belongs from middle socioeconomic status. He is vegetarian. His has completed B.com. Total income of him is 15,000 /month. He is from Hindu religion so he is following all customs, rituals as pre Hindu. He has habit of smoking and chewing tobacco. He looks young, well body built and always enthusiastic to perform his tasks. Previousllly he did not look weak and lethargic than right now.
He is having good nature,responsibility towards his family members He says that I want everybody should be happy as well as healthy in my family this information given by family members.
FAMILY HISTORY: His family is very social and has good relation with society member. Family also very cooperative with all. He has two children one boy and one girl. He is belongs from middle socioeconomic status. Her wife is having history of hyper tension since 1 year. No other family members have no any major diseases like tuberculosis, ischemic heart diseases ,cancer ,asthma allergy ,etc, Family tree
Mr vanaraj 33 years
Mrs. Maya 30 years
Mast. Mayank 9 year
Ms. Hetal 6 year MALE
FEMALE
SOCIOECONOMIC HISTORY:
He is belongs from middle socioeconomic status. He was staying in village upto 22 years then after marriage he was shifted to Ahmadabad. Total income family is 15,000 /month. He is from Hindu religion so he is following all customs, rituals as pre Hindu. His family is very social and has good relation with society member. Family also very cooperative. They have good relationship with neighbor.
PHYSICAL ASSESSMENT GORDEN’S DATA BASE ASSESSMENT: Height :159cm Weight:45 kg Vital signs; • • • • • Respiration Pulse Temperature :14breaths/min : 68beats/min :100 F
Blood pressure: 100/50 mm of hg RBS : 410mg/dl
B) ORIENTATION TO UNIT: Patient made to oriented as following: • • • • Call system Side rails on bed : it is beside the patient. :yes
Meal /cafeteria hours : as patient is unconscious ryles tube feeding is given. Visitation Policy : Yes, explained to the relatives that the visiting hours is from 12 noon to 1 pm and in evening time is 6 to 7 pm.
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Urination
: Foleys catheter is inserted.
C) Health pattern Assessment: 1 .Reason for Hospitalization Vomiting since 2 days and abdominal pain since 1 day, history of altered consciousness since today morning, fever 2 .Recent illness or exposure to communicable disease My patient had no previously any communicable disease. 3 .Previous Hospitalization or surgeries Before 5 years he had jaundice, and before 3 years he had falisparum malaria also for that he had 2 times hospitalize for treatment. 4 .What other problems you had? He had complains had breathlessness along with chronic coughing, also he had suffered from chronic constipation for that he was taking some ayurvedic tablets as per advised by ayurvedic doctor. 5. Things done to manage health: No necessary and adequate health steps were taken by individual in family to support him or by patient himself. 6 .Statement of patient’s general appearance Patient looks unconscious, not well oriented to time, place, person and environment, not following verbal commands. 7. Tobacco use: He did not take tobacco in any kind of extra form except 10-15 bidis per day. 8. Allergies: No any allergy to any drug or no sensitivity to any other drugs. 9. Food: He likes to eat green leafy vegetables, fruits, chapatti and milk, pulses, salad etc; He has no any food allergy. 10. MEDICATION: • Inj Human insulin 15 units SC before lunch and before dinner
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Inj cefotaxim 2 g every 4 hrly. Inj voveran 25 mg IV bd Inj Pantodac 40 mg IV bd Inj dopamine 200mg+NS 40 cc IV 4 ml /hour running in infusion pump. Inj Noradrenaline 2mg+NS 48 cc IV running in infusion pump Inj Emset 4 mg IV 8 hrly Inj DNS 40 ml IV running in pint.
11. Have you been taking your medications as been prescribed? Yes 12. Other patient data: not applicable
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NUTRITION / METABOLIC ASSESSMENT:
Patient is on ventilator so he is on nil per mouth status. • •
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SUPPLEMENTS: No any supplements to be taken by the client PATTERN OF DAILY FOOD/FLUID INTAKE He is on nil per mouth. So IV fluid is going on like DNS and RL. APPETITE: normal WEIGHT LOSS/GAIN: loss 1.2 kg NAUSEA/VOMITING: yes GI PAIN: no CONDITION OF THE ORAL MUCUS MEMBRANE : good no ulcers or nfection DENTAL CONDITION: all teeth is present DENTURES: present SKIN :warm and dry TURGOR: fragile COLOR: pale EDEMA : no WOUND/DRAIN /DRESSINGS: no
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SKIN PROBLEMS: no I V’S: yes OTHER PATIENT DATA: --
3. ELIMINATION:
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ABDOMINAL TENDERNESS: present BOWEL SOUNDS: Not applicable STOMA: Not applicable ANY PROBLEM WITH HEMORROIDS/INVOLUNTARY STOOL: Not applicable USUAL BOWEL PATTERN Client usually goes in the morning for the defecation usually once a day.
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DATE OF LAST BM :12-11- 10 IF PROBLEM DESCRIBE :no problem USE OF ANY THING TO MANAGE BOWELS: not applicable USUAL URINARY PATTERN Client is usually suffering from diabetes .so she is having excessive thirst and same way urination. So he goes frequently for the urination
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LAST VOID: in the morning IF PROBLEM DESCRIBE: no problem PERSPIRATION/NOCTURAL SWEATS: Not applicable OTHER PATIENT DATA: Not applicable
4. ACTIVITY /EXERCISE
CARDIOVASCULAR STATUS
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PERIPHERAL PULSES: 82beats/min NEUROVASCULAR CHECK: capillary refill 2 sec CHEST PAIN/RADIATION: no
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JUGULAR VEIN DISTENTION: no HX OF MURMUR: no PACEMAKER: no PRESENCE OF AV SHUNT: no ATRIOVENOUS BRUIT : no HEMODYNAMIC MONITORING: SPO2- 96% BLOOD PRESSURE- 110/30 mm of hg RESPIRATION – 15breaths of ventilator TEMPERATURE- 100 F PULSE- 82 beats/min ECG- normal -Normal sinus rhythm of heart rate ,no tachycardia,no tachypna,bradycardia or no bradypnea -Left ventricular ejection fraction is 60% -No evidence of chest pain .
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PERIPHERALSMEAR EXAMINATION: wbc shows polymorphoneclear leucocytosis
RESPIRATORY STATUS
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RESPIRATORY PATTERN: gasping respiration after kept on ventilator normal breathing pattern S.O.B ON EXERTION: present OTHER: Not applicable LUNG SOUNDS: On auscultation normal lung sounds were present. Along with few crepitation sounds in rright and left lower zone of Lungs. No evidence of rhonchi or wheezing sound. USE OF ACCESSORY MUSCLES:present COUGH/PRODUCTION : on ventilator patient having excessive secretions that are sticky and thick in consistency ,white in colour,so daily every 4 hrly
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suctioning is done regularly ,taking care Of him without harming to mucous membranes and to facilitate cough secretions nebulization is given along with duolin and budecort alternately
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RESPIRATORY TUBES: endotracheal tube inserted and attach with ventilator VENTILATORY ASSISTANCE: yes
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COGNITIVWE OR PERCEPTUAL ASSESSMENT:
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LEVEL OF CONSCIOUOSNESS: on admission he was unconscious and disoriented ,so he was intubaed on 8th November at 11o’clock
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BEHAVIOUR: He is unconscious. So I cannot able to assess the behaviour. HISTORY OF EPILEPSY AND SEIZURES:Not present and no history of parkinson’s disease • REFLEXES: o o o Eye: Pupil size Normal in both eyes Pupillary reaction: equal in both eyes Accomodation: within normal limits No deviation found either in right or in left eye Not having cataract or previous eye operation No myopia or hypermetropia HANDGRASP GAG REFLEX : present : present
SWALLOWING REFLEX :present
• MOVEMENT OF EXTREMITIES: PRESENT
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SENSORIUM FUNCTION: Eyes/sight : no cataract in both yes but hypermetropia is present
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Ears/hearing Nose/smell
: He is unconscious. So I cannot able to assess :He is unconscious. So I cannot able to assess : He is unconscious. So I cannot able to assess :no problem not present
• Tongue/taste Numbness/tingling • • • PAIN Dizziness
He has abdominal pain before 2 days. • COGNITION ASSESSMENT
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Primary language: gujarati Speech deficit: No problem Aid : not using Any learning difficulties: Now not able to learn new things
SLEEP OR REST ASSESSMENT:
At home adequate amount of sleep,but disturbed sometimes only because frequent urination at night.
7. SELF CONCEPT OR PERCEPTION:
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ARE THERE ANY WAYS YOU FEEL DIFFERENTLY ABOUT YOUR SELF SINCE YOU HAVE BEEN HOSPITALIZED OR ILL: Patient is unconscious
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DESCRIPTION OF NONVERBAL BEHAVIOUR: Patient is unconscious OTHER PATIENT DATA:--
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ROLE/RELATIONSHIP
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MARRITAL STATUS; MARRIED CHILDREN: two boys DO YOU LIVE ALONE/WITH FAMILY/OTHER: with family FAMILY FEELINGS REGARDING HOSPITALIZATION:her both the child is very attached to him and cares for him .they are worried about their father and participates in him care. They want that their father will be again healthy and independent. WHO ARE THE PEOPLE THAT WILL HELP YOU MOST AT THIS TIME: his wife ARE YOU PRESENTLY EMPLOYED: yes, get the information from his wife ARE YOU PRESENTLY IN SCHOOL: no OTHER PATIENT DATA:
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9. COPING OR STRESS:
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HAVE EXPERIENCED ANY RECENT SITUATION IN ADDITION TO YOUR ILLNESS : not applicable IF YES PLEASE DESCRIBE: not applicable ARE THERE ANY WAYS WE CAN BE OF ASSISTANCE : not applicable HOW DO YOU USUALLY MANAGE THE STRESS: not applicable WHAT DO YOU DO FOR RELAXATION: not applicable SUPPORT GROUPS /COUNCELLLING RESOURCES USED: not applicable
10. VALUE/BELIEF WILL ILLNESS/HOSPITALIZATION INTERFERE WITH ANY OF THE FOLLOWING?
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SPIRITUAL OR RELIGIOUS PRACTICES: not applicable CULTURAL BELIEFS OR PRACTICES: not applicable
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FAMILY TRADITIONS: not applicable WOULD YOU LIKE TO CONTACT HOSPITAL AUTHORITY : not applicable OTHER PATIENT DATA:--
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11. IMPRRESSION: -Possible nursing diagnostic concepts to consider for care planning; • • • • • impaired gas exchange related to excessive mucus secretion as evidenced by frequent suctioning and low saturation of oxygen. Alteration in thermoregulation, fever related to presence of infection and due to low immunity as evidenced by checking temperature. Activity intolerance related to immobility as evidenced by stiffness of the joints. Imbalanced nutrition less than body requirement related to vomiting and nausea as evidenced by checking skin turgor. Risk for infection related to invasive procedure like insertion of ET tube as evidence by increased WBC count.
ANATOMY AND PHYSIOLOGY:
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Anatomy and function of the Pancreas
Pancreas glandular organ that secretes digestive enzymes and hormones. In humans, the pancreas is a yellowish organ about 7 in. (17.8 cm) long and 1.5 in. (3.8 cm) wide. It lies beneath the stomach and is connected to the small intestine at the duodenum. Most of the pancreatic tissue consists of grapelike clusters of cells that produce a clear fluid (pancreatic juice) that flows into the duodenum through a common duct along with bile from the liver. Pancreatic juice contains three digestive
enzymes: tryptase, amylase, and lipase, that, along with intestinal enzymes, complete the digestion of proteins, carbohydrates, and fats, respectively. Scattered among the enzyme-producing cells of the pancreas are small groups of endocrine cells, called the islets of Langerhans, that secrete two hormones, insulin and glucagon. The pancreatic islets contain several types of cells: alpha-2 cells, which produce the hormone glucagon; beta cells, which manufacture the hormone insulin; and alpha-1 cells, which produce the regulatory agent somatostatin. These hormones are secreted directly into the bloodstream, and together, they regulate the level of glucose in the blood. Insulin lowers the blood sugar level and increases the amount of glycogen (stored carbohydrate) in the liver; glucagon has the opposite action. Failure of the insulin-secreting cells to function properly results in diabetes, which can occur in two major forms, the division being between juvenile onset and onset in maturity. Pancreatic cancer has a particularly high mortality rate, and patients with a family history of the disease sometimes have the pancreas removed if precancerous cysts are present in the organ. Every cell in the human body needs energy in order to function. The body’s primary energy source is glucose, a simple sugar resulting from the digestion of foods containing carbohydrates (sugars and starches). Glucose from the digested food circulates in the blood as a ready energy source for any cells that need it. Insulin is a hormone or chemical produced by cells in the pancreas, an organ located behind the stomach. Insulin bonds to a receptor site on the outside of cell and acts like a key to open a doorway into the cell through which glucose can enter. Some of the glucose can be converted to concentrated energy sources like glycogen or fatty acids and saved for later use. When there is not enough insulin produced or when the doorway no longer recognizes the insulin key, glucose stays in the blood rather entering the cells.
INSULIN EFFECTS: HOW DOES INSULIN LOWER BLOOD SUGAR LEVELS Although insulin plays a vital role in the regulation of carbohydrate, fat and protein metabolism, it is probably best known for its ability to lower blood sugar levels. So how exactly does insulin reduce blood glucose levels? Immediately after a meal, sugar in the blood stream stimulates the secretion of insulin from the pancreas which then goes about clearing the sugar from the blood stream by promoting its absorption, utilization and storage by tissues of the body. Insulin effects mainly include:
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Promoting glucose uptake and use by muscles Promoting glucose uptake, use and storage by liver cells
Insulin Effects on Muscles to Reduce Blood Glucose Levels The first thing to understand is that glucose is a substance used by cells to produce energy required for activities of the body. Muscle cells do not usually utilize blood glucose, even when its concentration is high in circulation, preferring instead to use fatty acids to produce energy required by them. But under the influence of insulin, muscle cells rapidly absorb glucose and use it to fuel their actions. This happens immediately after a meal when insulin secretion is high. The only other time muscle cells use up glucose in the blood stream, even in the absence of insulin, is during exercise.
But what happens when the body is resting after a meal and insulin is actively transporting sugar into muscle cells? These glucose molecules are strung together to form glycogen, the storage form of glucose. Glycogen is stored in muscle tissue for later use, especially when muscles require lots of energy for short spurts of strenuous activity. In a similar manner, insulin helps glucose uptake and use by most other cells in the body, except the brain cells. Insulin Effects on Liver to Lower Blood Sugar One of the important functions of the liver is to act as a storehouse for energy. Under the influence of insulin, most of the glucose absorbed from a meal is transported into the liver where it is converted into and stored as glycogen. When the body requires energy in between meals, glycogen from the liver stores is broken down and glucose released into circulation. High blood glucose levels cause insulin secretion which promotes glucose storage in the liver, whereas low blood sugar levels inhibit insulin secretion, causing glucose stores to be broken down and returned to the blood. Blood Glucose Regulation – Conversion of Glucose into Fatty Acids Unfortunately, there is a limit to the capacity of the liver to store glycogen. So what happens when this limit is exceeded? Insulin causes the excess glucose to be converted into fatty acids which are then released into circulation as very low density lipooroteins (VLDL). These find their way to fat stores in the body called adipose tissue. This goes a long way in explaining how high carbohydrate diets cause fat deposition in the body. Insulin also promotes fat deposition by uptake of glucose by adipose (fat) cells where it is used to form the glycerol part of the fat molecule. Insulin Effects on Brain Cells Interestingly, brain cells do not depend on insulin at all. They only use glucose for energy production (unlike other cells which can also use fatty acids and other substrates) which they directly absorb from the blood, independent of insulin. When the glucose level falls below a critical level, brain cells suffer by going into hypoglycemic shock. In diabetes mellitus, where there is either a lack of insulin or resistance to its action, glucose metabolism is severely impaired. Most of the cells are unable to use glucose, except, fortunately, the brain cells. Insulin effects on muscle, liver and adipose tissue help lower blood sugar levels by glucose uptake, use and storage. Insulin therefore plays a vital role in blood glucose regulation and maintaining normal blood glucose levels.
DIABETIC KETOACIDOSIS
INTRODUCTION Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism. The most common causes are underlying infection, disruption of insulin treatment, and new onset of diabetes.Diabetic ketoacidosis is typically characterized by hyperglycemia over 300 mg/dL, low bicarbonate level (<15 mEq/L), and acidosis (pH <7.30) with ketonemia and ketonuria. While definitions vary, moderate DKA can be categorized by pH <7.2 and serum bicarbonate <10 mEq/L, whereas severe DKA has pH <7.1 and bicarbonate <5 mEq/L. Mental status changes can be seen with mild-to-moderate DKA with more severe deterioration in mental status typical with moderate-to-severe DKA. DEFINATION Diabetic ketoacidosis is a complication of diabetes that occurs when the body cannot use sugar (glucose) as a fuel source because the body has no insulin or not enough insulin, and fat is used instead. Byproducts of fat breakdown, called ketones, build up in the body. Diabetic ketoacidosis is a metabolic derangement in TYPE 1 diabetis that results from a deficiency of insulin . highly acidic ketone bodies are formed , resulting in acidosis, usally requires hospitalisation for treatment and is usally caused by nonadherence to the insulin regiman , concurrent illness, or infection. INCIDENCE AS PER TEXT BOOK • How ever , mortality rates have declined during this same period. It occur most frequently in teenagers and older adults. Diabetic ketoacidosis occurs primarily in patients with type 1 diabetes. The incidence is roughly 2 episodes per 100 patient years of diabetes, with about 3% of patients with type 1 diabetes initially presenting with diabetic ketoacidosis. It can occur in patients with type 2 diabetes as well; however, this is less common. People with type 2 diabetes can develop ketoacidosis, but it is rare. It is AS PER PATIENT My patient is 33 years old.
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usually triggered by a severe illness. People of Hispanic and AfricanAmerican ethnicity seem to be more likely to have ketoacidosis as a complication of type 2 diabetes. ETIOLOGY AS PER TEXT BOOK • • • • • The most common scenarios for diabetic ketoacidosis are underlying or concomitant infection (40%) missed insulin treatments (25%), and newly diagnosed previously unknown diabetes (15%). Other associated causes make up roughly 20% in the various series. Urinary tract infections (UTIs) are the single most common infection associated with diabetic ketoacidosis But many other associated illnesses need to be considered as well.
AS PER PATIENT
Myocardial infarction Cerebrovascular accident Complicated pregnancy Trauma Stress Cocaine Surgery Heavy use of concentrated carbohydrate beverages such as sodas and sports drinks Acromegaly Idiopathic (20-30%) Dental abscess1
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As fats are broken down, acids called ketones build up in the blood and urine. In high levels, ketones are poisonous. This condition is known as ketoacidosis
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Blood glucose levels rise (usually higher than 300 mg/dL) because the liver produces glucose to try to combat the problem. However the cells cannot pull in that glucose without insulin.
PATHOPHYSIOLOGY:
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Many of the underlying pathophysiologic disturbances in diabetic ketoacidosis (DKA) are directly measurable by the clinician and need to be monitored throughout the course of treatment. Close attention to clinical laboratory data allows for tracking of the underlying acidosis and hyperglycemia as well as prevention of common potentially lethal complications such as hypoglycemia, hyponatremia, and hypokalemia. The absence of insulin, the primary anabolic hormone, means that tissues such as muscle, fat, and liver do not take up glucose. Counterregulatory hormones, such as glucagon, growth hormone, and catecholamines, enhance triglyceride breakdown into free fatty acids and gluconeogenesis, which is the main cause for the elevation in serum glucose level in diabetic ketoacidosis. Beta-oxidation of these free fatty acids leads to increased formation of ketone bodies. Overall, metabolism in diabetic ketoacidosis shifts from the
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normal fed state characterized by carbohydrate metabolism to a fasting state characterized by fat metabolism. • Secondary consequences of the primary metabolic derangements in diabetic ketoacidosis include an ensuing metabolic acidosis as the ketone bodies produced by beta-oxidation of free fatty acids deplete extracellular and cellular acid buffers. The hyperglycemia-induced osmotic diuresis depletes sodium, potassium, phosphates, and water as well as ketones and glucose. Patients are often profoundly dehydrated and have a significantly depleted potassium level (as high as 5 mEq per kg of body weight). A normal or even elevated serum potassium concentration may be seen due to the extracellular shift of potassium in acidotic conditions, and this very poorly reflects the patient's total potassium stores. The serum potassium concentration can drop precipitously once insulin treatment is started, so great care must be taken to repeatedly monitor serum levels. Urinary loss of ketoanions with brisk diuresis and intact renal function may also lead to a component of hyperchloremic metabolic acidosis.
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CLINICAL MANIFESTATION AS PER TEXT BOOK
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AS PER PATIENT
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Classic symptoms of hyperglycemia o Thirst o Polyuria, polydipsia o Nocturia Other symptoms o Generalized weakness
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Malaise/lethargy Nausea/vomiting Decreased perspiration Fatigue Anorexia or increased appetite Confusion Symptoms of associated infections and conditions o Fever o Dysuria o Chills o Chest pain o Abdominal pain o Shortness of breath
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General signs o Ill appearance o Dry skin o Labored respirations o Dry mucous membranes o Decreased skin turgor o Decreased reflexes Vital signs o Tachycardia o Hypotension o Tachypnea o Hypothermia o Fever, if infection Specific signs o Ketotic breath (fruity, with acetone smell) o Confusion o Coma o Abdominal tenderness
DIAGNOSTIC TEST AS PER TEXT BOOK AS PER PATIENT
History collection Physical examination Ketone testing may be used in type 1
diabetes to screen for early ketoacidosis. The ketones test is done using a urine sample. Ketone testing is usually done at the following times:
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When the blood sugar is higher than 240 mg/dL During an illness such as pneumonia, heart attack, or stroke When nausea or vomiting occur During pregnancy Ketonuria
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Other tests that may be done to diagnose ketoacidosis include:
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Arterial blood gas Blood glucose test Blood pressure measurement Amylase blood test Potassium blood test
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This disease may also affect the results of the following tests:
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CO2 CSF collection Potassium urine test Magnesium blood test Phosphorus blood test Sodium blood test Sodium urine test Urine pH
MEDICAL MANAGEMENT AS PER TEXT BOOK The main aims in the treatment of diabetic ketoacidosis are replacing the lost fluids and electrolytes while suppressing AS PER PATIENT
the high blood sugars and ketone production with insulin. Admission to an intensive care unit or similar high-dependency area or ward for close observation may be necessary. Fluid replacement
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The amount of fluid depends on the estimated degree of dehydration. If dehydration is so severe as to cause shock (severely decreased blood pressure with insufficient blood supply to the body's organs), or a depressed level of consciousness, rapid infusion of saline (1 liter for adults, 10 ml/kg in repeated doses for children) is recommended to restore circulating volume. Slower rehydration based on calculated water and sodium shortage may be possible if the dehydration is moderate, and again saline is the recommended fluid. Very mild ketoacidosis with no associated vomiting and mild dehydration may be treated with oral rehydration and subcutaneous rather than intravenous insulin under observation for signs of deterioration. A special but unusual consideration is cardiogenic shock, where the blood pressure is decreased not due to dehydration but due to inability of the heart to pump blood through the blood vessels. This situation requires ICU admission, monitoring of the central venous pressure (which requires the insertion of a central venous catheter in a large upper body vein), and the administration of medication that increases the heart pumping action and blood pressure.[1]
Insulin • Some guidelines recommend a bolus (initial large dose) of insulin of 0.1 unit of insulin per kilogram of body weight. This can be administered immediately after the potassium level is known to be higher than 3.3 mmol/l; if the level is any lower, administering insulin could lead to a dangerously low potassium level (see below). Other guidelines recommend delaying the initiation of insulin until fluids have been administrered. In general, insulin is given at 0.1 unit/kg per hour to reduce the blood sugars and suppress ketone production. Guidelines differ as to which dose to use when blood sugar levels start falling; some recommend reducing the dose of insulin once glucose falls below 16.6 mmol/l (300 mg/dl)[1] but other recommend infusing glucose in addition to saline to allow for ongoing infusion of higher doses of insulin.[9][5]
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Potassium
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Potassium levels can fluctuate severely during the treatment of DKA, because insulin decreases potassium levels in the blood by redistributing it into cells. Serum potassium levels are initially often mildly raised even though total body potassium is depleted—as potassium from the intracellular space would have been shifted to the extracellular space in an exchange for hydrogen ions that accumulate extracellularly in acidosis of DKA. A large part of the shifted extracellular potassium would have been lost in
urine because of osmotic diuresis. Hypokalemia (low blood potassium concentration) often follows treatment. This increases the risk of dangerous irregularities in the heart rate. Therefore, continuous observation of the heart rate is recommended,[9] as well as repeated measurement of the potassium levels and addition of potassium to the intravenous fluids once levels fall below 5.3 mmol/l. If potassium levels fall below 3.3 mmol/l, insulin administration may need to be interrupted to allow correction of the hypokalemia.[1] Bicarbonate
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The administration of sodium bicarbonate solution to rapidly improve the acid levels in the blood is controversial. There is little evidence that it improves outcomes beyond standard therapy, and indeed some evidence that while it may improve the acidity of the blood, it may actually worsen acidity inside the body's cells and increase the risk of certain complications. Its use is therefore discouraged,[2][5][10] although some guidelines recommend it for extreme acidosis (pH<6.9), and smaller amounts for severe acidosis (pH 6.9– 7.0).
Cerebral edema
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Cerebral edema, if associated with coma, often necessitates admission to intensive care, artificial ventilation, and close observation. The administration of fluids is slowed. The ideal treatment of cerebral edema in DKA is not established, but intravenous mannitol and hypertonic saline (3%) are used—
as in some other forms of cerebral edema—in an attempt to reduce the swelling.[2] Resolution • Resolution of DKA is defined as general improvement in the symptoms, such as the ability to tolerate oral nutrition and fluids, normalization of blood acidity (pH>7.3), and absence of ketones in blood (<1 mmol/l) or urine. Once this has been achieved, insulin may be switched to the usual subcutaneously administrered regimen, one hour after which the intravenous administration can be discontinued. In patients with suspected ketosisprone type 2 diabetes, determination of antibodies against glutamic acid decarboxylase and islet cells may aid in the decision whether to continue insulin administration long-term (if antibodies are detected), or whether to attempt treatment with oral medication as in type 2 diabetes.
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POSSIBLE COMPLICATIONS
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Fluid buildup in the brain (cerebral edema) Heart attack and death of bowel tissue due to low blood pressure Renal failure
PREVENTION
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People with diabetes should learn to recognize the early warning signs and symptoms of ketoacidosis. In people with infections or who are on insulin pump therapy, measuring urine ketones can give more information than glucose measurements alone. Insulin pump users need to check often to see that insulin is still flowing through the tubing, and that there are no blockages, kinks, or disconnections.
TOPIC:case study
SUBMITTED TO PROF.MR.YONATAN LECTURER J G COLLEGE OF NURSING SUBMITTED BY BINAL JOSHI F Y MSC NURSING J G COLLEGE OF NURSING
PATIENT’S BIODATA: NAME AGE SEX : Mr. prakash shah : 33years : male : Dr. Biren Hashvadan
DOCTOR’S UNIT
DATE OF ADMISSION : 8 /11/2010 REGISTRATION NO ADDRESS : 68099 : 45,bandhan society Sarkhej, Ahmedabad- 380082 MOBILE NO MARITAL STATUS OCCUPATION RELIGION NATIONALITY DIAGNOSIS : 9567244120 : Married : company worker : Hindu : Indian : congestive heart failure HISTORY OF PATIENT: CHIEF COMPLAINS: Mr. vanaraj was admitted in medical intensive care unit of shalby hospital with the complaints of vomiting since 2 days and abdominal pain since 1 day, history of altered consciousness since today morning,, fever is also present. At the time of admission vital signs. Respiration – gasping respiration. Pulse – feasible pulse present. Temperature- 100F. Blood pressure- 80/ 40 mm of hg. Emergency treatment given to the patient that is endotrachel intubation done and ventilator support given by AMBU bag.
PRESENT HISTORY Today patient is unconscious, not oriented to time, place and person, now also he is on ventilator support .Central venous catheter is inserted using triple lumen catheter into internal jugular vein ,iv fluids RL is going on. Chest leads applied on chest and attach with cardiac monitoring. Cardiac monitoring is continuing. Today 1 episodes of vomiting in morning and nausea also present. Blood pressure is decreased 80/40. So inj dopamine is going on via infusion pump. Urinary catheter is present, urine output is 1800ml /day. His temperature sometimes get high, it was 101 F, So antipyretic injection febrinil was given to him, Vital signs • • • • • Respiration Pulse Temperature :14breaths/min : 68beats/min :100 F
Blood pressure: 100/50 mm of hg RBS : 410mg/dl
PAST HISTORY: Mr.vanaraj has past history of diabetes mellitus since 10 years he is taking tab metformin 10 mg . no any other medical illness. He has no any surgical past history. Before 5 years he had jaundice ,and before 3 years he had falisparum malaria also for that he had 2 times hospitalize for treatment. He had complains had breathlessness along with chronic coughing, also he had suffered from chronic constipation for that he was taking some ayurvedic tablets as per advised by ayurvedic doctor.
PERSONAL HISTORY: Mr.vanaraj ,he was admitted in Medical ICU on 8th November,2010 ;he is working in company .His wife is housewife. He has two children one boy and one girl. He is belongs from middle socioeconomic status. He is vegetarian. His has completed B.com. Total income of him is 15,000 /month. He is from Hindu religion so he is following all customs, rituals as pre Hindu. He has habit of smoking and chewing tobacco. He looks young, well body built and always enthusiastic to perform his tasks. Previousllly he did not look weak and lethargic than right now.
He is having good nature,responsibility towards his family members He says that I want everybody should be happy as well as healthy in my family this information given by family members.
FAMILY HISTORY: His family is very social and has good relation with society member. Family also very cooperative with all. He has two children one boy and one girl. He is belongs from middle socioeconomic status. Her wife is having history of hyper tension since 1 year. No other family members have no any major diseases like tuberculosis, ischemic heart diseases ,cancer ,asthma allergy ,etc, Family tree
Mr vanaraj 33 years
Mrs. Maya 30 years
Mast. Mayank 9 year
Ms. Hetal 6 year MALE
FEMALE
SOCIOECONOMIC HISTORY:
He is belongs from middle socioeconomic status. He was staying in village upto 22 years then after marriage he was shifted to Ahmadabad. Total income family is 15,000 /month. He is from Hindu religion so he is following all customs, rituals as pre Hindu. His family is very social and has good relation with society member. Family also very cooperative. They have good relationship with neighbor.
PHYSICAL ASSESSMENT GORDEN’S DATA BASE ASSESSMENT: Height :159cm Weight:45 kg Vital signs; • • • • • Respiration Pulse Temperature :14breaths/min : 68beats/min :100 F
Blood pressure: 100/50 mm of hg RBS : 410mg/dl
B) ORIENTATION TO UNIT: Patient made to oriented as following: • • • • Call system Side rails on bed : it is beside the patient. :yes
Meal /cafeteria hours : as patient is unconscious ryles tube feeding is given. Visitation Policy : Yes, explained to the relatives that the visiting hours is from 12 noon to 1 pm and in evening time is 6 to 7 pm.
•
Urination
: Foleys catheter is inserted.
C) Health pattern Assessment: 1 .Reason for Hospitalization Vomiting since 2 days and abdominal pain since 1 day, history of altered consciousness since today morning, fever 2 .Recent illness or exposure to communicable disease My patient had no previously any communicable disease. 3 .Previous Hospitalization or surgeries Before 5 years he had jaundice, and before 3 years he had falisparum malaria also for that he had 2 times hospitalize for treatment. 4 .What other problems you had? He had complains had breathlessness along with chronic coughing, also he had suffered from chronic constipation for that he was taking some ayurvedic tablets as per advised by ayurvedic doctor. 5. Things done to manage health: No necessary and adequate health steps were taken by individual in family to support him or by patient himself. 6 .Statement of patient’s general appearance Patient looks unconscious, not well oriented to time, place, person and environment, not following verbal commands. 7. Tobacco use: He did not take tobacco in any kind of extra form except 10-15 bidis per day. 8. Allergies: No any allergy to any drug or no sensitivity to any other drugs. 9. Food: He likes to eat green leafy vegetables, fruits, chapatti and milk, pulses, salad etc; He has no any food allergy. 10. MEDICATION: • Inj Human insulin 15 units SC before lunch and before dinner
• • • • • • •
Inj cefotaxim 2 g every 4 hrly. Inj voveran 25 mg IV bd Inj Pantodac 40 mg IV bd Inj dopamine 200mg+NS 40 cc IV 4 ml /hour running in infusion pump. Inj Noradrenaline 2mg+NS 48 cc IV running in infusion pump Inj Emset 4 mg IV 8 hrly Inj DNS 40 ml IV running in pint.
11. Have you been taking your medications as been prescribed? Yes 12. Other patient data: not applicable
2.
NUTRITION / METABOLIC ASSESSMENT:
Patient is on ventilator so he is on nil per mouth status. • •
• • • • • • • • • • • •
SUPPLEMENTS: No any supplements to be taken by the client PATTERN OF DAILY FOOD/FLUID INTAKE He is on nil per mouth. So IV fluid is going on like DNS and RL. APPETITE: normal WEIGHT LOSS/GAIN: loss 1.2 kg NAUSEA/VOMITING: yes GI PAIN: no CONDITION OF THE ORAL MUCUS MEMBRANE : good no ulcers or nfection DENTAL CONDITION: all teeth is present DENTURES: present SKIN :warm and dry TURGOR: fragile COLOR: pale EDEMA : no WOUND/DRAIN /DRESSINGS: no
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SKIN PROBLEMS: no I V’S: yes OTHER PATIENT DATA: --
3. ELIMINATION:
• • • •
ABDOMINAL TENDERNESS: present BOWEL SOUNDS: Not applicable STOMA: Not applicable ANY PROBLEM WITH HEMORROIDS/INVOLUNTARY STOOL: Not applicable USUAL BOWEL PATTERN Client usually goes in the morning for the defecation usually once a day.
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• • •
DATE OF LAST BM :12-11- 10 IF PROBLEM DESCRIBE :no problem USE OF ANY THING TO MANAGE BOWELS: not applicable USUAL URINARY PATTERN Client is usually suffering from diabetes .so she is having excessive thirst and same way urination. So he goes frequently for the urination
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• • • •
LAST VOID: in the morning IF PROBLEM DESCRIBE: no problem PERSPIRATION/NOCTURAL SWEATS: Not applicable OTHER PATIENT DATA: Not applicable
4. ACTIVITY /EXERCISE
CARDIOVASCULAR STATUS
• • •
PERIPHERAL PULSES: 82beats/min NEUROVASCULAR CHECK: capillary refill 2 sec CHEST PAIN/RADIATION: no
• • • • •
JUGULAR VEIN DISTENTION: no HX OF MURMUR: no PACEMAKER: no PRESENCE OF AV SHUNT: no ATRIOVENOUS BRUIT : no HEMODYNAMIC MONITORING: SPO2- 96% BLOOD PRESSURE- 110/30 mm of hg RESPIRATION – 15breaths of ventilator TEMPERATURE- 100 F PULSE- 82 beats/min ECG- normal -Normal sinus rhythm of heart rate ,no tachycardia,no tachypna,bradycardia or no bradypnea -Left ventricular ejection fraction is 60% -No evidence of chest pain .
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•
PERIPHERALSMEAR EXAMINATION: wbc shows polymorphoneclear leucocytosis
RESPIRATORY STATUS
• • • •
RESPIRATORY PATTERN: gasping respiration after kept on ventilator normal breathing pattern S.O.B ON EXERTION: present OTHER: Not applicable LUNG SOUNDS: On auscultation normal lung sounds were present. Along with few crepitation sounds in rright and left lower zone of Lungs. No evidence of rhonchi or wheezing sound. USE OF ACCESSORY MUSCLES:present COUGH/PRODUCTION : on ventilator patient having excessive secretions that are sticky and thick in consistency ,white in colour,so daily every 4 hrly
• •
suctioning is done regularly ,taking care Of him without harming to mucous membranes and to facilitate cough secretions nebulization is given along with duolin and budecort alternately
• •
RESPIRATORY TUBES: endotracheal tube inserted and attach with ventilator VENTILATORY ASSISTANCE: yes
5.
COGNITIVWE OR PERCEPTUAL ASSESSMENT:
•
LEVEL OF CONSCIOUOSNESS: on admission he was unconscious and disoriented ,so he was intubaed on 8th November at 11o’clock
• •
BEHAVIOUR: He is unconscious. So I cannot able to assess the behaviour. HISTORY OF EPILEPSY AND SEIZURES:Not present and no history of parkinson’s disease • REFLEXES: o o o Eye: Pupil size Normal in both eyes Pupillary reaction: equal in both eyes Accomodation: within normal limits No deviation found either in right or in left eye Not having cataract or previous eye operation No myopia or hypermetropia HANDGRASP GAG REFLEX : present : present
SWALLOWING REFLEX :present
• MOVEMENT OF EXTREMITIES: PRESENT
• •
SENSORIUM FUNCTION: Eyes/sight : no cataract in both yes but hypermetropia is present
• •
Ears/hearing Nose/smell
: He is unconscious. So I cannot able to assess :He is unconscious. So I cannot able to assess : He is unconscious. So I cannot able to assess :no problem not present
• Tongue/taste Numbness/tingling • • • PAIN Dizziness
He has abdominal pain before 2 days. • COGNITION ASSESSMENT
• • • • 6.
Primary language: gujarati Speech deficit: No problem Aid : not using Any learning difficulties: Now not able to learn new things
SLEEP OR REST ASSESSMENT:
At home adequate amount of sleep,but disturbed sometimes only because frequent urination at night.
7. SELF CONCEPT OR PERCEPTION:
•
ARE THERE ANY WAYS YOU FEEL DIFFERENTLY ABOUT YOUR SELF SINCE YOU HAVE BEEN HOSPITALIZED OR ILL: Patient is unconscious
•
DESCRIPTION OF NONVERBAL BEHAVIOUR: Patient is unconscious OTHER PATIENT DATA:--
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8.
ROLE/RELATIONSHIP
• • • •
MARRITAL STATUS; MARRIED CHILDREN: two boys DO YOU LIVE ALONE/WITH FAMILY/OTHER: with family FAMILY FEELINGS REGARDING HOSPITALIZATION:her both the child is very attached to him and cares for him .they are worried about their father and participates in him care. They want that their father will be again healthy and independent. WHO ARE THE PEOPLE THAT WILL HELP YOU MOST AT THIS TIME: his wife ARE YOU PRESENTLY EMPLOYED: yes, get the information from his wife ARE YOU PRESENTLY IN SCHOOL: no OTHER PATIENT DATA:
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•
9. COPING OR STRESS:
• • • • • •
HAVE EXPERIENCED ANY RECENT SITUATION IN ADDITION TO YOUR ILLNESS : not applicable IF YES PLEASE DESCRIBE: not applicable ARE THERE ANY WAYS WE CAN BE OF ASSISTANCE : not applicable HOW DO YOU USUALLY MANAGE THE STRESS: not applicable WHAT DO YOU DO FOR RELAXATION: not applicable SUPPORT GROUPS /COUNCELLLING RESOURCES USED: not applicable
10. VALUE/BELIEF WILL ILLNESS/HOSPITALIZATION INTERFERE WITH ANY OF THE FOLLOWING?
• •
SPIRITUAL OR RELIGIOUS PRACTICES: not applicable CULTURAL BELIEFS OR PRACTICES: not applicable
• •
FAMILY TRADITIONS: not applicable WOULD YOU LIKE TO CONTACT HOSPITAL AUTHORITY : not applicable OTHER PATIENT DATA:--
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11. IMPRRESSION: -Possible nursing diagnostic concepts to consider for care planning; • • • • • impaired gas exchange related to excessive mucus secretion as evidenced by frequent suctioning and low saturation of oxygen. Alteration in thermoregulation, fever related to presence of infection and due to low immunity as evidenced by checking temperature. Activity intolerance related to immobility as evidenced by stiffness of the joints. Imbalanced nutrition less than body requirement related to vomiting and nausea as evidenced by checking skin turgor. Risk for infection related to invasive procedure like insertion of ET tube as evidence by increased WBC count.
ANATOMY AND PHYSIOLOGY:
•
Anatomy and function of the Pancreas
Pancreas glandular organ that secretes digestive enzymes and hormones. In humans, the pancreas is a yellowish organ about 7 in. (17.8 cm) long and 1.5 in. (3.8 cm) wide. It lies beneath the stomach and is connected to the small intestine at the duodenum. Most of the pancreatic tissue consists of grapelike clusters of cells that produce a clear fluid (pancreatic juice) that flows into the duodenum through a common duct along with bile from the liver. Pancreatic juice contains three digestive
enzymes: tryptase, amylase, and lipase, that, along with intestinal enzymes, complete the digestion of proteins, carbohydrates, and fats, respectively. Scattered among the enzyme-producing cells of the pancreas are small groups of endocrine cells, called the islets of Langerhans, that secrete two hormones, insulin and glucagon. The pancreatic islets contain several types of cells: alpha-2 cells, which produce the hormone glucagon; beta cells, which manufacture the hormone insulin; and alpha-1 cells, which produce the regulatory agent somatostatin. These hormones are secreted directly into the bloodstream, and together, they regulate the level of glucose in the blood. Insulin lowers the blood sugar level and increases the amount of glycogen (stored carbohydrate) in the liver; glucagon has the opposite action. Failure of the insulin-secreting cells to function properly results in diabetes, which can occur in two major forms, the division being between juvenile onset and onset in maturity. Pancreatic cancer has a particularly high mortality rate, and patients with a family history of the disease sometimes have the pancreas removed if precancerous cysts are present in the organ. Every cell in the human body needs energy in order to function. The body’s primary energy source is glucose, a simple sugar resulting from the digestion of foods containing carbohydrates (sugars and starches). Glucose from the digested food circulates in the blood as a ready energy source for any cells that need it. Insulin is a hormone or chemical produced by cells in the pancreas, an organ located behind the stomach. Insulin bonds to a receptor site on the outside of cell and acts like a key to open a doorway into the cell through which glucose can enter. Some of the glucose can be converted to concentrated energy sources like glycogen or fatty acids and saved for later use. When there is not enough insulin produced or when the doorway no longer recognizes the insulin key, glucose stays in the blood rather entering the cells.
INSULIN EFFECTS: HOW DOES INSULIN LOWER BLOOD SUGAR LEVELS Although insulin plays a vital role in the regulation of carbohydrate, fat and protein metabolism, it is probably best known for its ability to lower blood sugar levels. So how exactly does insulin reduce blood glucose levels? Immediately after a meal, sugar in the blood stream stimulates the secretion of insulin from the pancreas which then goes about clearing the sugar from the blood stream by promoting its absorption, utilization and storage by tissues of the body. Insulin effects mainly include:
• •
Promoting glucose uptake and use by muscles Promoting glucose uptake, use and storage by liver cells
Insulin Effects on Muscles to Reduce Blood Glucose Levels The first thing to understand is that glucose is a substance used by cells to produce energy required for activities of the body. Muscle cells do not usually utilize blood glucose, even when its concentration is high in circulation, preferring instead to use fatty acids to produce energy required by them. But under the influence of insulin, muscle cells rapidly absorb glucose and use it to fuel their actions. This happens immediately after a meal when insulin secretion is high. The only other time muscle cells use up glucose in the blood stream, even in the absence of insulin, is during exercise.
But what happens when the body is resting after a meal and insulin is actively transporting sugar into muscle cells? These glucose molecules are strung together to form glycogen, the storage form of glucose. Glycogen is stored in muscle tissue for later use, especially when muscles require lots of energy for short spurts of strenuous activity. In a similar manner, insulin helps glucose uptake and use by most other cells in the body, except the brain cells. Insulin Effects on Liver to Lower Blood Sugar One of the important functions of the liver is to act as a storehouse for energy. Under the influence of insulin, most of the glucose absorbed from a meal is transported into the liver where it is converted into and stored as glycogen. When the body requires energy in between meals, glycogen from the liver stores is broken down and glucose released into circulation. High blood glucose levels cause insulin secretion which promotes glucose storage in the liver, whereas low blood sugar levels inhibit insulin secretion, causing glucose stores to be broken down and returned to the blood. Blood Glucose Regulation – Conversion of Glucose into Fatty Acids Unfortunately, there is a limit to the capacity of the liver to store glycogen. So what happens when this limit is exceeded? Insulin causes the excess glucose to be converted into fatty acids which are then released into circulation as very low density lipooroteins (VLDL). These find their way to fat stores in the body called adipose tissue. This goes a long way in explaining how high carbohydrate diets cause fat deposition in the body. Insulin also promotes fat deposition by uptake of glucose by adipose (fat) cells where it is used to form the glycerol part of the fat molecule. Insulin Effects on Brain Cells Interestingly, brain cells do not depend on insulin at all. They only use glucose for energy production (unlike other cells which can also use fatty acids and other substrates) which they directly absorb from the blood, independent of insulin. When the glucose level falls below a critical level, brain cells suffer by going into hypoglycemic shock. In diabetes mellitus, where there is either a lack of insulin or resistance to its action, glucose metabolism is severely impaired. Most of the cells are unable to use glucose, except, fortunately, the brain cells. Insulin effects on muscle, liver and adipose tissue help lower blood sugar levels by glucose uptake, use and storage. Insulin therefore plays a vital role in blood glucose regulation and maintaining normal blood glucose levels.
DIABETIC KETOACIDOSIS
INTRODUCTION Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism. The most common causes are underlying infection, disruption of insulin treatment, and new onset of diabetes.Diabetic ketoacidosis is typically characterized by hyperglycemia over 300 mg/dL, low bicarbonate level (<15 mEq/L), and acidosis (pH <7.30) with ketonemia and ketonuria. While definitions vary, moderate DKA can be categorized by pH <7.2 and serum bicarbonate <10 mEq/L, whereas severe DKA has pH <7.1 and bicarbonate <5 mEq/L. Mental status changes can be seen with mild-to-moderate DKA with more severe deterioration in mental status typical with moderate-to-severe DKA. DEFINATION Diabetic ketoacidosis is a complication of diabetes that occurs when the body cannot use sugar (glucose) as a fuel source because the body has no insulin or not enough insulin, and fat is used instead. Byproducts of fat breakdown, called ketones, build up in the body. Diabetic ketoacidosis is a metabolic derangement in TYPE 1 diabetis that results from a deficiency of insulin . highly acidic ketone bodies are formed , resulting in acidosis, usally requires hospitalisation for treatment and is usally caused by nonadherence to the insulin regiman , concurrent illness, or infection. INCIDENCE AS PER TEXT BOOK • How ever , mortality rates have declined during this same period. It occur most frequently in teenagers and older adults. Diabetic ketoacidosis occurs primarily in patients with type 1 diabetes. The incidence is roughly 2 episodes per 100 patient years of diabetes, with about 3% of patients with type 1 diabetes initially presenting with diabetic ketoacidosis. It can occur in patients with type 2 diabetes as well; however, this is less common. People with type 2 diabetes can develop ketoacidosis, but it is rare. It is AS PER PATIENT My patient is 33 years old.
•
•
usually triggered by a severe illness. People of Hispanic and AfricanAmerican ethnicity seem to be more likely to have ketoacidosis as a complication of type 2 diabetes. ETIOLOGY AS PER TEXT BOOK • • • • • The most common scenarios for diabetic ketoacidosis are underlying or concomitant infection (40%) missed insulin treatments (25%), and newly diagnosed previously unknown diabetes (15%). Other associated causes make up roughly 20% in the various series. Urinary tract infections (UTIs) are the single most common infection associated with diabetic ketoacidosis But many other associated illnesses need to be considered as well.
AS PER PATIENT
Myocardial infarction Cerebrovascular accident Complicated pregnancy Trauma Stress Cocaine Surgery Heavy use of concentrated carbohydrate beverages such as sodas and sports drinks Acromegaly Idiopathic (20-30%) Dental abscess1
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As fats are broken down, acids called ketones build up in the blood and urine. In high levels, ketones are poisonous. This condition is known as ketoacidosis
•
Blood glucose levels rise (usually higher than 300 mg/dL) because the liver produces glucose to try to combat the problem. However the cells cannot pull in that glucose without insulin.
PATHOPHYSIOLOGY:
•
Many of the underlying pathophysiologic disturbances in diabetic ketoacidosis (DKA) are directly measurable by the clinician and need to be monitored throughout the course of treatment. Close attention to clinical laboratory data allows for tracking of the underlying acidosis and hyperglycemia as well as prevention of common potentially lethal complications such as hypoglycemia, hyponatremia, and hypokalemia. The absence of insulin, the primary anabolic hormone, means that tissues such as muscle, fat, and liver do not take up glucose. Counterregulatory hormones, such as glucagon, growth hormone, and catecholamines, enhance triglyceride breakdown into free fatty acids and gluconeogenesis, which is the main cause for the elevation in serum glucose level in diabetic ketoacidosis. Beta-oxidation of these free fatty acids leads to increased formation of ketone bodies. Overall, metabolism in diabetic ketoacidosis shifts from the
•
normal fed state characterized by carbohydrate metabolism to a fasting state characterized by fat metabolism. • Secondary consequences of the primary metabolic derangements in diabetic ketoacidosis include an ensuing metabolic acidosis as the ketone bodies produced by beta-oxidation of free fatty acids deplete extracellular and cellular acid buffers. The hyperglycemia-induced osmotic diuresis depletes sodium, potassium, phosphates, and water as well as ketones and glucose. Patients are often profoundly dehydrated and have a significantly depleted potassium level (as high as 5 mEq per kg of body weight). A normal or even elevated serum potassium concentration may be seen due to the extracellular shift of potassium in acidotic conditions, and this very poorly reflects the patient's total potassium stores. The serum potassium concentration can drop precipitously once insulin treatment is started, so great care must be taken to repeatedly monitor serum levels. Urinary loss of ketoanions with brisk diuresis and intact renal function may also lead to a component of hyperchloremic metabolic acidosis.
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CLINICAL MANIFESTATION AS PER TEXT BOOK
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AS PER PATIENT
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Classic symptoms of hyperglycemia o Thirst o Polyuria, polydipsia o Nocturia Other symptoms o Generalized weakness
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Malaise/lethargy Nausea/vomiting Decreased perspiration Fatigue Anorexia or increased appetite Confusion Symptoms of associated infections and conditions o Fever o Dysuria o Chills o Chest pain o Abdominal pain o Shortness of breath
o o o o o o
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General signs o Ill appearance o Dry skin o Labored respirations o Dry mucous membranes o Decreased skin turgor o Decreased reflexes Vital signs o Tachycardia o Hypotension o Tachypnea o Hypothermia o Fever, if infection Specific signs o Ketotic breath (fruity, with acetone smell) o Confusion o Coma o Abdominal tenderness
DIAGNOSTIC TEST AS PER TEXT BOOK AS PER PATIENT
History collection Physical examination Ketone testing may be used in type 1
diabetes to screen for early ketoacidosis. The ketones test is done using a urine sample. Ketone testing is usually done at the following times:
• • • • •
When the blood sugar is higher than 240 mg/dL During an illness such as pneumonia, heart attack, or stroke When nausea or vomiting occur During pregnancy Ketonuria
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Other tests that may be done to diagnose ketoacidosis include:
• • • • •
Arterial blood gas Blood glucose test Blood pressure measurement Amylase blood test Potassium blood test
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This disease may also affect the results of the following tests:
• • • • • • • •
CO2 CSF collection Potassium urine test Magnesium blood test Phosphorus blood test Sodium blood test Sodium urine test Urine pH
MEDICAL MANAGEMENT AS PER TEXT BOOK The main aims in the treatment of diabetic ketoacidosis are replacing the lost fluids and electrolytes while suppressing AS PER PATIENT
the high blood sugars and ketone production with insulin. Admission to an intensive care unit or similar high-dependency area or ward for close observation may be necessary. Fluid replacement
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•
The amount of fluid depends on the estimated degree of dehydration. If dehydration is so severe as to cause shock (severely decreased blood pressure with insufficient blood supply to the body's organs), or a depressed level of consciousness, rapid infusion of saline (1 liter for adults, 10 ml/kg in repeated doses for children) is recommended to restore circulating volume. Slower rehydration based on calculated water and sodium shortage may be possible if the dehydration is moderate, and again saline is the recommended fluid. Very mild ketoacidosis with no associated vomiting and mild dehydration may be treated with oral rehydration and subcutaneous rather than intravenous insulin under observation for signs of deterioration. A special but unusual consideration is cardiogenic shock, where the blood pressure is decreased not due to dehydration but due to inability of the heart to pump blood through the blood vessels. This situation requires ICU admission, monitoring of the central venous pressure (which requires the insertion of a central venous catheter in a large upper body vein), and the administration of medication that increases the heart pumping action and blood pressure.[1]
Insulin • Some guidelines recommend a bolus (initial large dose) of insulin of 0.1 unit of insulin per kilogram of body weight. This can be administered immediately after the potassium level is known to be higher than 3.3 mmol/l; if the level is any lower, administering insulin could lead to a dangerously low potassium level (see below). Other guidelines recommend delaying the initiation of insulin until fluids have been administrered. In general, insulin is given at 0.1 unit/kg per hour to reduce the blood sugars and suppress ketone production. Guidelines differ as to which dose to use when blood sugar levels start falling; some recommend reducing the dose of insulin once glucose falls below 16.6 mmol/l (300 mg/dl)[1] but other recommend infusing glucose in addition to saline to allow for ongoing infusion of higher doses of insulin.[9][5]
•
Potassium
•
Potassium levels can fluctuate severely during the treatment of DKA, because insulin decreases potassium levels in the blood by redistributing it into cells. Serum potassium levels are initially often mildly raised even though total body potassium is depleted—as potassium from the intracellular space would have been shifted to the extracellular space in an exchange for hydrogen ions that accumulate extracellularly in acidosis of DKA. A large part of the shifted extracellular potassium would have been lost in
urine because of osmotic diuresis. Hypokalemia (low blood potassium concentration) often follows treatment. This increases the risk of dangerous irregularities in the heart rate. Therefore, continuous observation of the heart rate is recommended,[9] as well as repeated measurement of the potassium levels and addition of potassium to the intravenous fluids once levels fall below 5.3 mmol/l. If potassium levels fall below 3.3 mmol/l, insulin administration may need to be interrupted to allow correction of the hypokalemia.[1] Bicarbonate
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The administration of sodium bicarbonate solution to rapidly improve the acid levels in the blood is controversial. There is little evidence that it improves outcomes beyond standard therapy, and indeed some evidence that while it may improve the acidity of the blood, it may actually worsen acidity inside the body's cells and increase the risk of certain complications. Its use is therefore discouraged,[2][5][10] although some guidelines recommend it for extreme acidosis (pH<6.9), and smaller amounts for severe acidosis (pH 6.9– 7.0).
Cerebral edema
•
Cerebral edema, if associated with coma, often necessitates admission to intensive care, artificial ventilation, and close observation. The administration of fluids is slowed. The ideal treatment of cerebral edema in DKA is not established, but intravenous mannitol and hypertonic saline (3%) are used—
as in some other forms of cerebral edema—in an attempt to reduce the swelling.[2] Resolution • Resolution of DKA is defined as general improvement in the symptoms, such as the ability to tolerate oral nutrition and fluids, normalization of blood acidity (pH>7.3), and absence of ketones in blood (<1 mmol/l) or urine. Once this has been achieved, insulin may be switched to the usual subcutaneously administrered regimen, one hour after which the intravenous administration can be discontinued. In patients with suspected ketosisprone type 2 diabetes, determination of antibodies against glutamic acid decarboxylase and islet cells may aid in the decision whether to continue insulin administration long-term (if antibodies are detected), or whether to attempt treatment with oral medication as in type 2 diabetes.
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POSSIBLE COMPLICATIONS
• • •
Fluid buildup in the brain (cerebral edema) Heart attack and death of bowel tissue due to low blood pressure Renal failure
PREVENTION
•
•
People with diabetes should learn to recognize the early warning signs and symptoms of ketoacidosis. In people with infections or who are on insulin pump therapy, measuring urine ketones can give more information than glucose measurements alone. Insulin pump users need to check often to see that insulin is still flowing through the tubing, and that there are no blockages, kinks, or disconnections.
