SlideShare uma empresa Scribd logo
1 de 47
ACUTE COMPLICATIONS OF
DIABETES MELLITUS
Questions
• A 39 year old Male patient presented to you in emergency
department for Acute Abdomen with H/O
vomiting,Restlessness,Lethargy,dehydration.On palpation of
abdomen diffuse tenderness+,no guarding/rigidity.On
Auscultation Bowel sounds heard. On eliciting History you
detect the patient is a known diabetic and is on insulin and
because of frequent travelling he is poorly complaint with
insulin.Your first probable diagnosis
a)Acute cholecystitis
b)Perforative peritonitis
c)Diabetic Ketoacidosis
d)Intestinal Obstruction
Questions
• A 62 yr old Diabetic Male presented to the Emergency with H/O fever,Right
Hypochondrial Pain,tachycardia for 2 days.CT abdomen done image is shown
below
The possible diagnosis
a)Emphysematous nephritis
b)Emphysematous cholecystitis
c)Perforative peritonitis
d)Alcoholic pancreatitis
Questions
• A 42 yr old Male known Diabetic for past 11 years with HbA1C 10.0
referred from an ENT surgeon to you the physician as a case of chronic
otorrhea,otalgia with hearing loss and now presenting with facial
asymmetry a provisional diagnosis of Rt. Facial N. palsy is made. You
suspect an infective pathology.The Probable organism could be
a)Streptococcus pneumonia
b)Hemophilus influenza
c)Pseudomonas aeruginosa
d)Clostridium perfringens
Questions
• A 54 yr old lady who is a diabetic for 12 years brought with h/o orbital cellulitis,6th
Nerve palsy and anosmia presenting with the following clinical picture
the Drug of choice for this patient?
a)Piperacillin Tazobactem
b)Amphotericin B
c)Mitomycin C
d)Actinomycin D
• Diabetic ketoacidosis
• Non ketotic hyperglycemic hyperosmolar
coma
• Hypoglycaemia & Hypoglycaemic coma
• Infections
Hyperglycemia
Ketosis
Acidosis
*
Definition of Diabetic Ketoacidosis
7
DKA is defined as the presence of all three of
the following:
(i) Hyperglycemia (glucose >250 mg/dL)
(ii) Ketosis,
(iii) Acidemia (pH <7.3).
Williams textbook of endocrinology 10th edition
Role of Insulin
• Required for transport of glucose into:
– Muscle
– Adipose
– Liver
• Inhibits lipolysis
• Absence of insulin
– Glucose accumulates
in the blood.
– Uses amino acids
for gluconeogenesis
– Converts fatty acids into ketone bodies :
Acetone, Acetoacetate, β-hydroxybutyrate.
Electrolyte
LossesRenal Failure
Shock CV
Collapse
Insulin Deficiency
9
Hyperglycemia
Hyper-
osmolality
Lipolysis
FFAs
Acidosis
Ketones
CV
Collapse
Glycosuria
Dehydration
Diabetic Ketoacidosis: Pathophysiology
Unchecked gluconeogenesis  Hyperglycemia
Osmotic diuresis  Dehydration
Unchecked ketogenesis  Ketosis
Dissociation of ketone bodies into
hydrogen ion and anions

Anion-gap metabolic
acidosis
• Often a precipitating event is identified (infection, lack of insulin
administration)
Clinical Presentation of
Diabetic Ketoacidosis
History Physical Exam
• Thirst
• Polyuria
• Abdominal pain
• Nausea and/or vomiting
• Profound weakness
• Kussmaul respirations
• Fruity breath
• Tachycardia
• Dry mucous membranes
• Poor skin turgor
• Abdominal tenderness(may
resemble acute pancreatitis
or surgical abdomen)
Diabetic Ketoacidosis
PRECIPITATING EVENTS
Infection(Pneumonia / UTI / Gastroenteritis / Sepsis)
Inadequate insulin administration
Infarction(cerebral, coronary, mesenteric, peripheral)
Drugs (cocaine)
Pregnancy.
Harrison’s Principle of internal medicine 18th edition p2977
DIAGNOSIS LAB INVESTIGATIONS
Complete blood count
Serum ketones/ Urine ketones and sugar
Calculate serum osmolality and anion gap
Urinalysis and urine culture
Consider blood culture
Consider chest radiograph
Acid-base assessment
Williams textbook of endocrinology 10th edition
TREATMENT OF DKA
Initial hospital management
– Replace fluid and electrolytes
– IV Insulin therapy
– Watch for complications
– Treat causes
Once resolved
– Convert to home insulin regimen
– Prevent recurrence
TYPICAL BODY DEFICIT OF WATER AND ELECTROLYTES
FLUIDS
FLUID RESUSCITATION IS A CRITICAL PART OF
TREATING PATIENTS WITH DKA.
Intravenous solutions replace extravascular and
intravascular fluids and electrolyte losses.
They also dilute both the glucose level and the levels of
circulating counterregulatory hormones.
Fluid it self leads to correction of acidosis to some
extent
Insulin is needed to help switch from a catabolic state
to an anabolic state, with uptake of glucose in tissues
and the reduction of gluconeogenesis as well as free
fatty acid and ketone production
FLUID REPLACEMENT
Administer NS as indicated to maintain hemodynamic status, then follow general guidelines:
 NS for first 4 hr.
 Consider half NS thereafter.
 Change to D5 half NS when blood glucose ≤250 mg/dL.
Williams textbook of endocrinology 10th edition
Hours Volume
 1st half-hour to 1 hour 1 L
 2nd hr 1 L
 3rd hr 500 mL– 1 L
 4th hr 500 mL– 1 L
 5th hr 500 mL– 1 L
 Total 1st 5 hr 3.5 - 5 L
 6th–12th hr 250– 500 mL/hr
May need to adjust type and rate of fluid administration in the elderly and in patients with
congestive heart failure or renal failure.
INSULIN MANAGEMENT
 Regular insulin 10 U i.v. stat (for adults) or 0.15 U/kg i.v. stat.
 Start regular insulin infusion 0.1 U/kg per hour or 5 U per hour.
 Increase insulin by 1 U per hour every 1–2 hr if less than 10% decrease in
glucose or no improvement in acid-base status.
 Decrease insulin by 1–2 U per hour (0.05–0.1 U/kg per hour) when glucose
≤250 mg/dL and/or progressive improvement in clinical status with decrease
in glucose of >75 mg/dL per hour.
 Do not decrease insulin infusion to <1 U per hour.
Williams textbook of endocrinology 10th edition
INSULIN MANAGEMENT CONTD…
 Maintain glucose between 140 and 180 mg/dL.
 If blood sugar decreases to <80 mg/dL, stop insulin infusion for no more than
1 hr and restart infusion.
 If glucose drops consistently to <100 mg/dL, change i.v. fluids to D10 to
maintain blood glucose between 140 and 180 mg/dL.
 Once patient is able to eat, consider change to s.c. insulin:
 Overlap short-acting insulin s.c. and continue i.v. infusion for 1–2 hr.
 For patients with previous insulin dose: return to prior dose of insulin.
 For patients with newly diagnosed diabetes: full-dose s.c. insulin based on 0.6
U/kg per day.
Williams textbook of endocrinology 10th edition
POTASSIUM REPLACEMENT
 Do not administer potassium if serum potassium >5.5 mEq/L or patient is anuric.
 Use KCl but alternate with KPO4 if there is severe phosphate depletion and patient is unable to
take phosphate by mouth.
 Add i.v. potassium to each liter of fluid administered unless contraindicated.
Williams textbook of endocrinology 10th edition p 454
Serum K (mEq/L) Additional K required
3.5 - 4.0 - 40mEq/L
3.5–4.5 - 20mEq/L
4.5–5.5 - 10mEq/L
>5.5 - Stop K infusion
-Williams textbook of endocrinology 10th edition
BICARBONATE
• Clinical trials do not support the routine use of bicarbonate replacement
• HCO3 replacement and rapid reversal of acidosis can impair cardiac function, reduce tissue
oxygenation and promote hypokalemia and hypocalcemia.
• However in presence of severe acidosis pH<6.9,in hemodynamic instability with pH<7.1 and
hyperkaemia with ecg finding bicarbonate therapy considered
• In the presence of severe acidosis (arterial pH <6.9), the ADA advises bicarbonate [50 mmol/L
(meq/L) of sodium bicarbonate in 200 mL of sterile water with 10 meq/L KCl per hour for 2 h
until the pH is >7.0].
Williams textbook of endocrinology 10th edition p456
TREATMENT OF DKA
GLUCOSE ADMINISTRATION
 Plasma glucose reaches 250 mg/dl in DKA or 300
mg/dl in HHS,
 Decrease the insulin infusion rate to 0.05–0.1
unit/kg/h (3–6 units/h),
 Add dextrose (5–10%) to the intravenous fluids.
Maintain the above glucose values until acidosis in
DKA or mental obtundation and hyperosmolarity in
HHS are resolved
Williams textbook of endocrinology 10th edition p 455
Criteria for resolution of DKA
 glucose <200 mg/dl,
 serum bicarbonate ≥18 mEq/l, and
 venous pH of >7.3.
Once DKA is resolved, if the patient is NPO,
continue intravenous insulin and fluid
replacement and supplement with
subcutaneous regular insulin as needed every
4 h.
ONCE DKA RESOLVED…
• Most patients require 0.5-0.6 units/kg/day
• highly insulin resistant patients
– 0.8-1.0 units/kg/day
• Give subcutaneous insulin at least 2 hours prior to weaning insulin
infusion.
Williams textbook of endocrinology 10th edition p455
CLINICAL ERRORS
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 fluid when ketones still
present
Hypoglycemia
 Insufficient glucose administration.
Hyperglycemic-Hyperosmolar State (HHS)
HNC is a syndrome characterized by impaired
consciousness, sometimes accompanied by
seizures, extreme dehydration, , and extreme
hyperglycemia that is not accompanied by
ketoacidosis.
DKA HHS
Ketonemia/Ketonuria + Ketonemia/Ketonuria -
Serum Osmolality N Serum Osmolality >320mosm
pH<7.3 pH>7.3
S.Glucose >250mg/dL S.Glucose >600mg/dL
Physical examination
1. Severe dehydration is invariably present.
2. Various neurologic deficits (such as coma, transient
hemiparesis, hyperreflexia, and generalized areflexia) are
commonly present. Altered states of consciousness from
lethargy to coma are observed.
3. Findings associated with coexisting medical problems
(e.g., renal disease, cardiovascular disease) may be
evident.
Laboratory findings
1. Extreme hyperglycemia (blood glucose levels from 30 mmoll/l and
over are common.
2. A markedly elevated serum osmolality is present, usually in excess
of 350 mOsm/l. (Normal = 290 mOsm)
3. Serum ketones are usually not detectable, and patients are not
acidic.
4. Serum sodium may be high (if severe degree of dehydration is
present), normal, or high
5. Serum potassium levels may be high (secondary to the effects of
hyperosmolality) Low or normal
Treatment
This condition is a medical emergency and the patient
should be placed in an intensive care unit.
Many of the management techniques recommended for a
patient with DKA are applicable here as well.
The goals of therapy include:
• rehydration;
• reduction of hyperglycemia;
• electrolytes replacement;
• investigation of precipitating factors, treatment of
complications.
Hypoglycemia
It is a syndrome characterized by symptoms of
sympathetic nervous system stimulation or
central nervous system dysfunction that are
provoked by an abnormally low plasma
glucose level and it can occur at any time.
Precipitating factors
• irregular ingestion of food;
• extreme activity;
• alcohol ingestion;
• drug interaction;
• liver or renal disease;
• hypopituitarism and adrenal insufficiency.
HYPOGLYCEMIA
Pathophysiology of hypoglycaemia
Inhibition of
endogenous
insulin secretion
Counter-
regulatory
hormone
release
• Glucagon
• Adrenaline
Onset of
symptoms
• Autonomic
• Neuroglycopa
enic
Neurophysiologic
al dysfunction
• Evoked
responses
Widespread
EEG
changes
Cognitive
dysfunction
• Inability to
perform
complex
tasksSevere
neuroglycop
aenia
• Reduced
level of
consciosn
ess
• Convulsio
ns
• Coma
83 mg/dL
58–50 mg/dL
68 mg/dL
54–43 mg/dL 54 mg/dL 50 mg/dL
<27 mg/dL
Arterialisedvenousbloodglucoseconcentration
(mmol/L)
2.
0
3.
0
4.
0
1.
0
0
5.
0
Cryer et al. Diabetes Care 2003;26:1902–12
EEG, electroencephalogram
Physical examination
1. The skin is cold, moist.
2. Hyperreflexia can be elicited.
3. Hypoglycemic coma is commonly associated
with abnormally low body temperature
4. Patient may be unconscious.
Treatment
• The most effective treatment of an insulin reaction is the immediate
ingestion of a concentrated carbohydrate source, such as sugar, honey,
candy, or orange juice.
• Alternative methods for increasing blood glucose may be required when
the person having the reaction is unconscious or unable to swallow:
– Glucagon may be given intramuscularly or subcutaneously.
– In situations of severe or life-threatening hypoglycemia, it may be
necessary to administer glucose intravenously.
• BG = 40 mg%: Give
(100-40) x 0.8 = 60 x
0.8= 48 ml of IV 25%
Dextrose.
• Repeat BG q 15 mins
until BG > 70mg%.
Example • If BG < 70mg% : 25% dextrose as per
calculation. Check BG q15 mins
• If BG > 70mg% : Check BG q30 mins till
BG > 90mg%
• If BG > 90mg% : Check BG q1hrly, Hold
Infusion
• If BG > 140mg%: Restart infusion at 50%
of previous rate
BG ≤70 – Suspend Insulin, Give 25% Dextrose (100-BG) X 0.8**
Infections
Complement:
some studies have detected a deficiency of the C4 component in DM,this reduction of C4 is
probably associated with polymorphonuclear dysfunction and reduced cytokine response
Polymorphonuclear and mononuclear leukocytes:
Decreased mobilization of polymorphonuclear leukocytes, chemotaxis, and phagocytic activity
may occur during hyperglycemia.
hyperglycemic environment inhibits glucose-6-phosphate dehydrogenase (G6PD), increasing
apoptosis of polymorphonuclear leukocytes, and reducing polymorphonuclear leukocyte
transmigration
In tissues that do not need insulin for glucose transport, the increased intracellular glucose levels
are then metabolized, using NADPH as a cofactor and the low NADPH prevents the regeneration
of molecules that play a key role in antioxidant mechanisms of the cell, thereby increasing the
susceptibility to oxidative stress.
the glycated hemoglobin (HbA1c) is <8.0%, to maintain the proliferative function of CD4 T
lymphocytes and their response to antigens.
Infections• Respiratory infections
Streptococcus pneumoniae and influenza virus
• Tuberculosis
• Urinary infections
• Bacterial pyelonephritis
E.Coli & Proteus
• Emphysematous pyelonephritis
E.Coli & Proteus followed by enterobacter.
• Emphysematous cystitis
The most frequent pathogen is E. coli, followed by Enterobacter, Proteus, Klebsiella,
and Candida
• Perinephric abscess
gram-negative bacilli (predominantly E. coli) or polymicrobial infection
• Emphysematous cholecystitis
The emphysematous cholecystitis is more frequent in males with DM.The main
pathogens are Salmonella enteritidis and Campylobacter
• Invasive external otitis
Invasive external otitis is an infection of the external auditory canal that can extend to
the skull base and adjacent regions.It often affects elderly diabetic individuals and the
etiologic agent is usually Pseudomonas aeruginosa
Questions
• A 39 year old Male patient presented to you in emergency
department for Acute Abdomen with H/O
vomiting,Restlessness,Lethargy,dehydration.On palpation of
abdomen diffuse tenderness+,no guarding/rigidity.On
Auscultation Bowel sounds heard. On eliciting History you
detect the patient is a known diabetic and is on insulin and
because of frequent travelling he is poorly complaint with
insulin.Your first probable diagnosis
a)Acute cholecystitis
b)Perforative peritonitis
c)Diabetic Ketoacidosis
d)Intestinal Obstruction
Questions
• A 62 yr old Diabetic Male presented to the Emergency with H/O fever,Right
Hypochondrial Pain,tachycardia for 2 days.CT abdomen done image is shown
below
The possible diagnosis
a)Emphysematous nephritis
b)Emphysematous cholecystitis
c)Perforative peritonitis
d)Alcoholic pancreatitis
Questions
• A 42 yr old Male known Diabetic for past 11 years with HbA1C 10.0
referred from an ENT surgeon to you the physician as a case of chronic
otorrhea,otalgia with hearing loss and now presenting with facial
asymmetry a provisional diagnosis of Rt. Facial N. palsy is made. You
suspect an infective pathology.The Probable organism could be
a)Streptococcus pneumonia
b)Hemophilus influenza
c)Pseudomonas aeruginosa
d)Clostridium perfringens
Questions
• A 54 yr old lady who is a diabetic for 12 years brought with h/o orbital cellulitis,6th
Nerve palsy and anosmia presenting with the following clinical picture
the Drug of choice for this patient?
a)Piperacillin Tazobactem
b)Amphotericin B
c)Mitomycin C
d)Actinomycin D
Acute complications of diabetes mellitus

Mais conteúdo relacionado

Mais procurados

BILIARY DYSKINESIA
BILIARY DYSKINESIA BILIARY DYSKINESIA
BILIARY DYSKINESIA shreya patel
 
NEPHRITIC SYNDROME / APSGN IN CHILDREN
NEPHRITIC SYNDROME / APSGN IN CHILDREN NEPHRITIC SYNDROME / APSGN IN CHILDREN
NEPHRITIC SYNDROME / APSGN IN CHILDREN Sajjad Sabir
 
Chronic cholecystitis & Jaundice
Chronic cholecystitis & JaundiceChronic cholecystitis & Jaundice
Chronic cholecystitis & JaundiceMuhammad Eimaduddin
 
Hyperglycemic hyperosmolar state hhs
Hyperglycemic hyperosmolar state hhsHyperglycemic hyperosmolar state hhs
Hyperglycemic hyperosmolar state hhsMEEQAT HOSPITAL
 
Obstructive jaundice
Obstructive jaundiceObstructive jaundice
Obstructive jaundiceSilah Aysha
 
Chronic hepatitis
Chronic hepatitis Chronic hepatitis
Chronic hepatitis ikramdr01
 
Hyperglycemic hyperosmolar
Hyperglycemic hyperosmolarHyperglycemic hyperosmolar
Hyperglycemic hyperosmolar941531003
 
Chronic complications of diabetes mellitus
Chronic complications of diabetes mellitusChronic complications of diabetes mellitus
Chronic complications of diabetes mellitusHamza AlGhamdi
 
Chronic pancreatitis
Chronic pancreatitisChronic pancreatitis
Chronic pancreatitisikramdr01
 
Malabsorption syndrome
Malabsorption syndromeMalabsorption syndrome
Malabsorption syndromeNikhil Gupta
 
Diagnosis and Treatment of Ascites
Diagnosis and Treatment of AscitesDiagnosis and Treatment of Ascites
Diagnosis and Treatment of AscitesWaleed El-Refaey
 
Adrenal insufficiency
Adrenal insufficiencyAdrenal insufficiency
Adrenal insufficiencyDJ CrissCross
 
acute pancreatitis
acute pancreatitisacute pancreatitis
acute pancreatitisssn zhd
 

Mais procurados (20)

BILIARY DYSKINESIA
BILIARY DYSKINESIA BILIARY DYSKINESIA
BILIARY DYSKINESIA
 
NEPHRITIC SYNDROME / APSGN IN CHILDREN
NEPHRITIC SYNDROME / APSGN IN CHILDREN NEPHRITIC SYNDROME / APSGN IN CHILDREN
NEPHRITIC SYNDROME / APSGN IN CHILDREN
 
Hypocalcaemia
HypocalcaemiaHypocalcaemia
Hypocalcaemia
 
Hypokalemia
HypokalemiaHypokalemia
Hypokalemia
 
Chronic cholecystitis & Jaundice
Chronic cholecystitis & JaundiceChronic cholecystitis & Jaundice
Chronic cholecystitis & Jaundice
 
hypoglycemia
hypoglycemiahypoglycemia
hypoglycemia
 
Renal amyloidosis
Renal amyloidosisRenal amyloidosis
Renal amyloidosis
 
Dyslipidemia
DyslipidemiaDyslipidemia
Dyslipidemia
 
Hyperglycemic hyperosmolar state hhs
Hyperglycemic hyperosmolar state hhsHyperglycemic hyperosmolar state hhs
Hyperglycemic hyperosmolar state hhs
 
Alcoholic Hepatitis
Alcoholic HepatitisAlcoholic Hepatitis
Alcoholic Hepatitis
 
Obstructive jaundice
Obstructive jaundiceObstructive jaundice
Obstructive jaundice
 
Chronic hepatitis
Chronic hepatitis Chronic hepatitis
Chronic hepatitis
 
Hyperglycemic hyperosmolar
Hyperglycemic hyperosmolarHyperglycemic hyperosmolar
Hyperglycemic hyperosmolar
 
Chronic complications of diabetes mellitus
Chronic complications of diabetes mellitusChronic complications of diabetes mellitus
Chronic complications of diabetes mellitus
 
Approach to ascites
Approach to ascitesApproach to ascites
Approach to ascites
 
Chronic pancreatitis
Chronic pancreatitisChronic pancreatitis
Chronic pancreatitis
 
Malabsorption syndrome
Malabsorption syndromeMalabsorption syndrome
Malabsorption syndrome
 
Diagnosis and Treatment of Ascites
Diagnosis and Treatment of AscitesDiagnosis and Treatment of Ascites
Diagnosis and Treatment of Ascites
 
Adrenal insufficiency
Adrenal insufficiencyAdrenal insufficiency
Adrenal insufficiency
 
acute pancreatitis
acute pancreatitisacute pancreatitis
acute pancreatitis
 

Semelhante a Acute complications of diabetes mellitus

Acute metabolic complications of diabetes mellitus
Acute metabolic complications of diabetes mellitusAcute metabolic complications of diabetes mellitus
Acute metabolic complications of diabetes mellitusPushpAnjali6
 
Diabetic Ketoacidosis
Diabetic KetoacidosisDiabetic Ketoacidosis
Diabetic KetoacidosisSof2050
 
Diabetes ketoacidosis
Diabetes ketoacidosisDiabetes ketoacidosis
Diabetes ketoacidosisOmkar Singh
 
Acute gastroenteritis and fluid management
Acute gastroenteritis and fluid managementAcute gastroenteritis and fluid management
Acute gastroenteritis and fluid managementProfMaila
 
DIABETIC KETO ACIDOSIS
DIABETIC KETO ACIDOSISDIABETIC KETO ACIDOSIS
DIABETIC KETO ACIDOSISAliya Emil
 
Diabetic keto acidosis
Diabetic keto acidosisDiabetic keto acidosis
Diabetic keto acidosisAliya Emil
 
Metabolic emergencies in diabetes mellitus
Metabolic emergencies in diabetes mellitusMetabolic emergencies in diabetes mellitus
Metabolic emergencies in diabetes mellitusNikhil Chougule
 
Diabetes Keto Acidosis management. .pptx
Diabetes Keto Acidosis management. .pptxDiabetes Keto Acidosis management. .pptx
Diabetes Keto Acidosis management. .pptxKTD Priyadarshani
 
Dka, hhns.pptx1
Dka, hhns.pptx1Dka, hhns.pptx1
Dka, hhns.pptx1arnoldtchu
 
diabetesketoacidosis about education pdf
diabetesketoacidosis about education pdfdiabetesketoacidosis about education pdf
diabetesketoacidosis about education pdfAkash782029
 
Metabolic-Emergencies.pptx
Metabolic-Emergencies.pptxMetabolic-Emergencies.pptx
Metabolic-Emergencies.pptxWengelRedkiss
 
dka-170312043320.pdfgghhfhdjrifgrgvfhdjfh
dka-170312043320.pdfgghhfhdjrifgrgvfhdjfhdka-170312043320.pdfgghhfhdjrifgrgvfhdjfh
dka-170312043320.pdfgghhfhdjrifgrgvfhdjfhMoviePics
 
Diabetic ketoacidosis (2)
Diabetic ketoacidosis (2)Diabetic ketoacidosis (2)
Diabetic ketoacidosis (2)Ali Alwan
 

Semelhante a Acute complications of diabetes mellitus (20)

Acute metabolic complications of diabetes mellitus
Acute metabolic complications of diabetes mellitusAcute metabolic complications of diabetes mellitus
Acute metabolic complications of diabetes mellitus
 
Diabetic Ketoacidosis
Diabetic KetoacidosisDiabetic Ketoacidosis
Diabetic Ketoacidosis
 
Diabetes ketoacidosis
Diabetes ketoacidosisDiabetes ketoacidosis
Diabetes ketoacidosis
 
Dka & hhs
Dka & hhsDka & hhs
Dka & hhs
 
Acute gastroenteritis and fluid management
Acute gastroenteritis and fluid managementAcute gastroenteritis and fluid management
Acute gastroenteritis and fluid management
 
Diabetic ketoacidosis
Diabetic ketoacidosisDiabetic ketoacidosis
Diabetic ketoacidosis
 
DIABETIC KETO ACIDOSIS
DIABETIC KETO ACIDOSISDIABETIC KETO ACIDOSIS
DIABETIC KETO ACIDOSIS
 
Diabetic keto acidosis
Diabetic keto acidosisDiabetic keto acidosis
Diabetic keto acidosis
 
Metabolic emergencies in diabetes mellitus
Metabolic emergencies in diabetes mellitusMetabolic emergencies in diabetes mellitus
Metabolic emergencies in diabetes mellitus
 
Diabetes Keto Acidosis management. .pptx
Diabetes Keto Acidosis management. .pptxDiabetes Keto Acidosis management. .pptx
Diabetes Keto Acidosis management. .pptx
 
Dka, hhns.pptx1
Dka, hhns.pptx1Dka, hhns.pptx1
Dka, hhns.pptx1
 
Dka
DkaDka
Dka
 
Diabetes ketoacidosis
Diabetes ketoacidosisDiabetes ketoacidosis
Diabetes ketoacidosis
 
diabetesketoacidosis about education pdf
diabetesketoacidosis about education pdfdiabetesketoacidosis about education pdf
diabetesketoacidosis about education pdf
 
Metabolic-Emergencies.pptx
Metabolic-Emergencies.pptxMetabolic-Emergencies.pptx
Metabolic-Emergencies.pptx
 
DKA.pptx
DKA.pptxDKA.pptx
DKA.pptx
 
Diabetic Ketoacidosis
Diabetic KetoacidosisDiabetic Ketoacidosis
Diabetic Ketoacidosis
 
dka-170312043320.pdfgghhfhdjrifgrgvfhdjfh
dka-170312043320.pdfgghhfhdjrifgrgvfhdjfhdka-170312043320.pdfgghhfhdjrifgrgvfhdjfh
dka-170312043320.pdfgghhfhdjrifgrgvfhdjfh
 
DKA
DKADKA
DKA
 
Diabetic ketoacidosis (2)
Diabetic ketoacidosis (2)Diabetic ketoacidosis (2)
Diabetic ketoacidosis (2)
 

Mais de ikramdr01

MI LOCALISATION.pptx
MI LOCALISATION.pptxMI LOCALISATION.pptx
MI LOCALISATION.pptxikramdr01
 
atrial fibrillation 2020 guidelines
atrial fibrillation 2020 guidelinesatrial fibrillation 2020 guidelines
atrial fibrillation 2020 guidelinesikramdr01
 
Wheezing dos and donts
Wheezing dos and dontsWheezing dos and donts
Wheezing dos and dontsikramdr01
 
Imaging in stroke
Imaging in strokeImaging in stroke
Imaging in strokeikramdr01
 
arterial disorders
arterial disordersarterial disorders
arterial disordersikramdr01
 
interstitial lung diseases
interstitial lung diseasesinterstitial lung diseases
interstitial lung diseasesikramdr01
 
Innovative gadgets in anesthesia and medicine
Innovative gadgets in anesthesia and medicine Innovative gadgets in anesthesia and medicine
Innovative gadgets in anesthesia and medicine ikramdr01
 
Clinical cardiology
Clinical cardiologyClinical cardiology
Clinical cardiologyikramdr01
 
Tuberculosis
TuberculosisTuberculosis
Tuberculosisikramdr01
 
Gestational diabetes mellitus
Gestational diabetes mellitusGestational diabetes mellitus
Gestational diabetes mellitusikramdr01
 
Gestational trophoblastic diseases
Gestational trophoblastic diseasesGestational trophoblastic diseases
Gestational trophoblastic diseasesikramdr01
 
Heart failure
Heart failure Heart failure
Heart failure ikramdr01
 
Scorpion sting
Scorpion stingScorpion sting
Scorpion stingikramdr01
 
Sarcoidosis and IgG4
Sarcoidosis and IgG4Sarcoidosis and IgG4
Sarcoidosis and IgG4ikramdr01
 
Neuropathic pain understanding and management
Neuropathic pain understanding and managementNeuropathic pain understanding and management
Neuropathic pain understanding and managementikramdr01
 
Optimizing heart failure management
Optimizing heart failure managementOptimizing heart failure management
Optimizing heart failure managementikramdr01
 
Kawasaki disease
Kawasaki diseaseKawasaki disease
Kawasaki diseaseikramdr01
 
bedside approach to common congenital heart diseases
bedside approach to common congenital heart diseasesbedside approach to common congenital heart diseases
bedside approach to common congenital heart diseasesikramdr01
 
Atrial fibrillation
Atrial fibrillation Atrial fibrillation
Atrial fibrillation ikramdr01
 
Infective endocarditis
Infective endocarditis Infective endocarditis
Infective endocarditis ikramdr01
 

Mais de ikramdr01 (20)

MI LOCALISATION.pptx
MI LOCALISATION.pptxMI LOCALISATION.pptx
MI LOCALISATION.pptx
 
atrial fibrillation 2020 guidelines
atrial fibrillation 2020 guidelinesatrial fibrillation 2020 guidelines
atrial fibrillation 2020 guidelines
 
Wheezing dos and donts
Wheezing dos and dontsWheezing dos and donts
Wheezing dos and donts
 
Imaging in stroke
Imaging in strokeImaging in stroke
Imaging in stroke
 
arterial disorders
arterial disordersarterial disorders
arterial disorders
 
interstitial lung diseases
interstitial lung diseasesinterstitial lung diseases
interstitial lung diseases
 
Innovative gadgets in anesthesia and medicine
Innovative gadgets in anesthesia and medicine Innovative gadgets in anesthesia and medicine
Innovative gadgets in anesthesia and medicine
 
Clinical cardiology
Clinical cardiologyClinical cardiology
Clinical cardiology
 
Tuberculosis
TuberculosisTuberculosis
Tuberculosis
 
Gestational diabetes mellitus
Gestational diabetes mellitusGestational diabetes mellitus
Gestational diabetes mellitus
 
Gestational trophoblastic diseases
Gestational trophoblastic diseasesGestational trophoblastic diseases
Gestational trophoblastic diseases
 
Heart failure
Heart failure Heart failure
Heart failure
 
Scorpion sting
Scorpion stingScorpion sting
Scorpion sting
 
Sarcoidosis and IgG4
Sarcoidosis and IgG4Sarcoidosis and IgG4
Sarcoidosis and IgG4
 
Neuropathic pain understanding and management
Neuropathic pain understanding and managementNeuropathic pain understanding and management
Neuropathic pain understanding and management
 
Optimizing heart failure management
Optimizing heart failure managementOptimizing heart failure management
Optimizing heart failure management
 
Kawasaki disease
Kawasaki diseaseKawasaki disease
Kawasaki disease
 
bedside approach to common congenital heart diseases
bedside approach to common congenital heart diseasesbedside approach to common congenital heart diseases
bedside approach to common congenital heart diseases
 
Atrial fibrillation
Atrial fibrillation Atrial fibrillation
Atrial fibrillation
 
Infective endocarditis
Infective endocarditis Infective endocarditis
Infective endocarditis
 

Último

❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...Sheetaleventcompany
 
Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...
Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...
Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...Cara Menggugurkan Kandungan 087776558899
 
Circulatory Shock, types and stages, compensatory mechanisms
Circulatory Shock, types and stages, compensatory mechanismsCirculatory Shock, types and stages, compensatory mechanisms
Circulatory Shock, types and stages, compensatory mechanismsMedicoseAcademics
 
Difference Between Skeletal Smooth and Cardiac Muscles
Difference Between Skeletal Smooth and Cardiac MusclesDifference Between Skeletal Smooth and Cardiac Muscles
Difference Between Skeletal Smooth and Cardiac MusclesMedicoseAcademics
 
Call Girls in Lucknow Just Call 👉👉8630512678 Top Class Call Girl Service Avai...
Call Girls in Lucknow Just Call 👉👉8630512678 Top Class Call Girl Service Avai...Call Girls in Lucknow Just Call 👉👉8630512678 Top Class Call Girl Service Avai...
Call Girls in Lucknow Just Call 👉👉8630512678 Top Class Call Girl Service Avai...soniyagrag336
 
ANATOMY AND PHYSIOLOGY OF RESPIRATORY SYSTEM.pptx
ANATOMY AND PHYSIOLOGY OF RESPIRATORY SYSTEM.pptxANATOMY AND PHYSIOLOGY OF RESPIRATORY SYSTEM.pptx
ANATOMY AND PHYSIOLOGY OF RESPIRATORY SYSTEM.pptxSwetaba Besh
 
💰Call Girl In Bangalore☎️7304373326💰 Call Girl service in Bangalore☎️Bangalor...
💰Call Girl In Bangalore☎️7304373326💰 Call Girl service in Bangalore☎️Bangalor...💰Call Girl In Bangalore☎️7304373326💰 Call Girl service in Bangalore☎️Bangalor...
💰Call Girl In Bangalore☎️7304373326💰 Call Girl service in Bangalore☎️Bangalor...Sheetaleventcompany
 
Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...
Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...
Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...Sheetaleventcompany
 
💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...
💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...
💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...Sheetaleventcompany
 
Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...
Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...
Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...Sheetaleventcompany
 
Call Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service Available
Call Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service AvailableCall Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service Available
Call Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service Availableperfect solution
 
Low Cost Call Girls Bangalore {9179660964} ❤️VVIP NISHA Call Girls in Bangalo...
Low Cost Call Girls Bangalore {9179660964} ❤️VVIP NISHA Call Girls in Bangalo...Low Cost Call Girls Bangalore {9179660964} ❤️VVIP NISHA Call Girls in Bangalo...
Low Cost Call Girls Bangalore {9179660964} ❤️VVIP NISHA Call Girls in Bangalo...Sheetaleventcompany
 
Call Girls Kathua Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Kathua Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Kathua Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Kathua Just Call 8250077686 Top Class Call Girl Service AvailableDipal Arora
 
💚Reliable Call Girls Chandigarh 💯Niamh 📲🔝8868886958🔝Call Girl In Chandigarh N...
💚Reliable Call Girls Chandigarh 💯Niamh 📲🔝8868886958🔝Call Girl In Chandigarh N...💚Reliable Call Girls Chandigarh 💯Niamh 📲🔝8868886958🔝Call Girl In Chandigarh N...
💚Reliable Call Girls Chandigarh 💯Niamh 📲🔝8868886958🔝Call Girl In Chandigarh N...Sheetaleventcompany
 
Bhawanipatna Call Girls 📞9332606886 Call Girls in Bhawanipatna Escorts servic...
Bhawanipatna Call Girls 📞9332606886 Call Girls in Bhawanipatna Escorts servic...Bhawanipatna Call Girls 📞9332606886 Call Girls in Bhawanipatna Escorts servic...
Bhawanipatna Call Girls 📞9332606886 Call Girls in Bhawanipatna Escorts servic...Dipal Arora
 
Call Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service Available
Call Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service AvailableCall Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service Available
Call Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service AvailableJanvi Singh
 
Call 8250092165 Patna Call Girls ₹4.5k Cash Payment With Room Delivery
Call 8250092165 Patna Call Girls ₹4.5k Cash Payment With Room DeliveryCall 8250092165 Patna Call Girls ₹4.5k Cash Payment With Room Delivery
Call 8250092165 Patna Call Girls ₹4.5k Cash Payment With Room DeliveryJyoti singh
 
Call Girls in Lucknow Just Call 👉👉 8875999948 Top Class Call Girl Service Ava...
Call Girls in Lucknow Just Call 👉👉 8875999948 Top Class Call Girl Service Ava...Call Girls in Lucknow Just Call 👉👉 8875999948 Top Class Call Girl Service Ava...
Call Girls in Lucknow Just Call 👉👉 8875999948 Top Class Call Girl Service Ava...Janvi Singh
 
Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...
Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...
Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...Sheetaleventcompany
 
Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...
Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...
Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...Sheetaleventcompany
 

Último (20)

❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
 
Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...
Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...
Cara Menggugurkan Kandungan Dengan Cepat Selesai Dalam 24 Jam Secara Alami Bu...
 
Circulatory Shock, types and stages, compensatory mechanisms
Circulatory Shock, types and stages, compensatory mechanismsCirculatory Shock, types and stages, compensatory mechanisms
Circulatory Shock, types and stages, compensatory mechanisms
 
Difference Between Skeletal Smooth and Cardiac Muscles
Difference Between Skeletal Smooth and Cardiac MusclesDifference Between Skeletal Smooth and Cardiac Muscles
Difference Between Skeletal Smooth and Cardiac Muscles
 
Call Girls in Lucknow Just Call 👉👉8630512678 Top Class Call Girl Service Avai...
Call Girls in Lucknow Just Call 👉👉8630512678 Top Class Call Girl Service Avai...Call Girls in Lucknow Just Call 👉👉8630512678 Top Class Call Girl Service Avai...
Call Girls in Lucknow Just Call 👉👉8630512678 Top Class Call Girl Service Avai...
 
ANATOMY AND PHYSIOLOGY OF RESPIRATORY SYSTEM.pptx
ANATOMY AND PHYSIOLOGY OF RESPIRATORY SYSTEM.pptxANATOMY AND PHYSIOLOGY OF RESPIRATORY SYSTEM.pptx
ANATOMY AND PHYSIOLOGY OF RESPIRATORY SYSTEM.pptx
 
💰Call Girl In Bangalore☎️7304373326💰 Call Girl service in Bangalore☎️Bangalor...
💰Call Girl In Bangalore☎️7304373326💰 Call Girl service in Bangalore☎️Bangalor...💰Call Girl In Bangalore☎️7304373326💰 Call Girl service in Bangalore☎️Bangalor...
💰Call Girl In Bangalore☎️7304373326💰 Call Girl service in Bangalore☎️Bangalor...
 
Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...
Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...
Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...
 
💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...
💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...
💚Call Girls In Amritsar 💯Anvi 📲🔝8725944379🔝Amritsar Call Girl No💰Advance Cash...
 
Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...
Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...
Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...
 
Call Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service Available
Call Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service AvailableCall Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service Available
Call Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service Available
 
Low Cost Call Girls Bangalore {9179660964} ❤️VVIP NISHA Call Girls in Bangalo...
Low Cost Call Girls Bangalore {9179660964} ❤️VVIP NISHA Call Girls in Bangalo...Low Cost Call Girls Bangalore {9179660964} ❤️VVIP NISHA Call Girls in Bangalo...
Low Cost Call Girls Bangalore {9179660964} ❤️VVIP NISHA Call Girls in Bangalo...
 
Call Girls Kathua Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Kathua Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Kathua Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Kathua Just Call 8250077686 Top Class Call Girl Service Available
 
💚Reliable Call Girls Chandigarh 💯Niamh 📲🔝8868886958🔝Call Girl In Chandigarh N...
💚Reliable Call Girls Chandigarh 💯Niamh 📲🔝8868886958🔝Call Girl In Chandigarh N...💚Reliable Call Girls Chandigarh 💯Niamh 📲🔝8868886958🔝Call Girl In Chandigarh N...
💚Reliable Call Girls Chandigarh 💯Niamh 📲🔝8868886958🔝Call Girl In Chandigarh N...
 
Bhawanipatna Call Girls 📞9332606886 Call Girls in Bhawanipatna Escorts servic...
Bhawanipatna Call Girls 📞9332606886 Call Girls in Bhawanipatna Escorts servic...Bhawanipatna Call Girls 📞9332606886 Call Girls in Bhawanipatna Escorts servic...
Bhawanipatna Call Girls 📞9332606886 Call Girls in Bhawanipatna Escorts servic...
 
Call Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service Available
Call Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service AvailableCall Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service Available
Call Girls Mussoorie Just Call 8854095900 Top Class Call Girl Service Available
 
Call 8250092165 Patna Call Girls ₹4.5k Cash Payment With Room Delivery
Call 8250092165 Patna Call Girls ₹4.5k Cash Payment With Room DeliveryCall 8250092165 Patna Call Girls ₹4.5k Cash Payment With Room Delivery
Call 8250092165 Patna Call Girls ₹4.5k Cash Payment With Room Delivery
 
Call Girls in Lucknow Just Call 👉👉 8875999948 Top Class Call Girl Service Ava...
Call Girls in Lucknow Just Call 👉👉 8875999948 Top Class Call Girl Service Ava...Call Girls in Lucknow Just Call 👉👉 8875999948 Top Class Call Girl Service Ava...
Call Girls in Lucknow Just Call 👉👉 8875999948 Top Class Call Girl Service Ava...
 
Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...
Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...
Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...
 
Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...
Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...
Chandigarh Call Girls Service ❤️🍑 9809698092 👄🫦Independent Escort Service Cha...
 

Acute complications of diabetes mellitus

  • 2. Questions • A 39 year old Male patient presented to you in emergency department for Acute Abdomen with H/O vomiting,Restlessness,Lethargy,dehydration.On palpation of abdomen diffuse tenderness+,no guarding/rigidity.On Auscultation Bowel sounds heard. On eliciting History you detect the patient is a known diabetic and is on insulin and because of frequent travelling he is poorly complaint with insulin.Your first probable diagnosis a)Acute cholecystitis b)Perforative peritonitis c)Diabetic Ketoacidosis d)Intestinal Obstruction
  • 3. Questions • A 62 yr old Diabetic Male presented to the Emergency with H/O fever,Right Hypochondrial Pain,tachycardia for 2 days.CT abdomen done image is shown below The possible diagnosis a)Emphysematous nephritis b)Emphysematous cholecystitis c)Perforative peritonitis d)Alcoholic pancreatitis
  • 4. Questions • A 42 yr old Male known Diabetic for past 11 years with HbA1C 10.0 referred from an ENT surgeon to you the physician as a case of chronic otorrhea,otalgia with hearing loss and now presenting with facial asymmetry a provisional diagnosis of Rt. Facial N. palsy is made. You suspect an infective pathology.The Probable organism could be a)Streptococcus pneumonia b)Hemophilus influenza c)Pseudomonas aeruginosa d)Clostridium perfringens
  • 5. Questions • A 54 yr old lady who is a diabetic for 12 years brought with h/o orbital cellulitis,6th Nerve palsy and anosmia presenting with the following clinical picture the Drug of choice for this patient? a)Piperacillin Tazobactem b)Amphotericin B c)Mitomycin C d)Actinomycin D
  • 6. • Diabetic ketoacidosis • Non ketotic hyperglycemic hyperosmolar coma • Hypoglycaemia & Hypoglycaemic coma • Infections
  • 7. Hyperglycemia Ketosis Acidosis * Definition of Diabetic Ketoacidosis 7 DKA is defined as the presence of all three of the following: (i) Hyperglycemia (glucose >250 mg/dL) (ii) Ketosis, (iii) Acidemia (pH <7.3). Williams textbook of endocrinology 10th edition
  • 8. Role of Insulin • Required for transport of glucose into: – Muscle – Adipose – Liver • Inhibits lipolysis • Absence of insulin – Glucose accumulates in the blood. – Uses amino acids for gluconeogenesis – Converts fatty acids into ketone bodies : Acetone, Acetoacetate, β-hydroxybutyrate.
  • 9. Electrolyte LossesRenal Failure Shock CV Collapse Insulin Deficiency 9 Hyperglycemia Hyper- osmolality Lipolysis FFAs Acidosis Ketones CV Collapse Glycosuria Dehydration
  • 10. Diabetic Ketoacidosis: Pathophysiology Unchecked gluconeogenesis  Hyperglycemia Osmotic diuresis  Dehydration Unchecked ketogenesis  Ketosis Dissociation of ketone bodies into hydrogen ion and anions  Anion-gap metabolic acidosis • Often a precipitating event is identified (infection, lack of insulin administration)
  • 11. Clinical Presentation of Diabetic Ketoacidosis History Physical Exam • Thirst • Polyuria • Abdominal pain • Nausea and/or vomiting • Profound weakness • Kussmaul respirations • Fruity breath • Tachycardia • Dry mucous membranes • Poor skin turgor • Abdominal tenderness(may resemble acute pancreatitis or surgical abdomen)
  • 12. Diabetic Ketoacidosis PRECIPITATING EVENTS Infection(Pneumonia / UTI / Gastroenteritis / Sepsis) Inadequate insulin administration Infarction(cerebral, coronary, mesenteric, peripheral) Drugs (cocaine) Pregnancy. Harrison’s Principle of internal medicine 18th edition p2977
  • 13. DIAGNOSIS LAB INVESTIGATIONS Complete blood count Serum ketones/ Urine ketones and sugar Calculate serum osmolality and anion gap Urinalysis and urine culture Consider blood culture Consider chest radiograph Acid-base assessment Williams textbook of endocrinology 10th edition
  • 14. TREATMENT OF DKA Initial hospital management – Replace fluid and electrolytes – IV Insulin therapy – Watch for complications – Treat causes Once resolved – Convert to home insulin regimen – Prevent recurrence TYPICAL BODY DEFICIT OF WATER AND ELECTROLYTES
  • 15. FLUIDS FLUID RESUSCITATION IS A CRITICAL PART OF TREATING PATIENTS WITH DKA. Intravenous solutions replace extravascular and intravascular fluids and electrolyte losses. They also dilute both the glucose level and the levels of circulating counterregulatory hormones. Fluid it self leads to correction of acidosis to some extent Insulin is needed to help switch from a catabolic state to an anabolic state, with uptake of glucose in tissues and the reduction of gluconeogenesis as well as free fatty acid and ketone production
  • 16. FLUID REPLACEMENT Administer NS as indicated to maintain hemodynamic status, then follow general guidelines:  NS for first 4 hr.  Consider half NS thereafter.  Change to D5 half NS when blood glucose ≤250 mg/dL. Williams textbook of endocrinology 10th edition Hours Volume  1st half-hour to 1 hour 1 L  2nd hr 1 L  3rd hr 500 mL– 1 L  4th hr 500 mL– 1 L  5th hr 500 mL– 1 L  Total 1st 5 hr 3.5 - 5 L  6th–12th hr 250– 500 mL/hr May need to adjust type and rate of fluid administration in the elderly and in patients with congestive heart failure or renal failure.
  • 17. INSULIN MANAGEMENT  Regular insulin 10 U i.v. stat (for adults) or 0.15 U/kg i.v. stat.  Start regular insulin infusion 0.1 U/kg per hour or 5 U per hour.  Increase insulin by 1 U per hour every 1–2 hr if less than 10% decrease in glucose or no improvement in acid-base status.  Decrease insulin by 1–2 U per hour (0.05–0.1 U/kg per hour) when glucose ≤250 mg/dL and/or progressive improvement in clinical status with decrease in glucose of >75 mg/dL per hour.  Do not decrease insulin infusion to <1 U per hour. Williams textbook of endocrinology 10th edition
  • 18. INSULIN MANAGEMENT CONTD…  Maintain glucose between 140 and 180 mg/dL.  If blood sugar decreases to <80 mg/dL, stop insulin infusion for no more than 1 hr and restart infusion.  If glucose drops consistently to <100 mg/dL, change i.v. fluids to D10 to maintain blood glucose between 140 and 180 mg/dL.  Once patient is able to eat, consider change to s.c. insulin:  Overlap short-acting insulin s.c. and continue i.v. infusion for 1–2 hr.  For patients with previous insulin dose: return to prior dose of insulin.  For patients with newly diagnosed diabetes: full-dose s.c. insulin based on 0.6 U/kg per day. Williams textbook of endocrinology 10th edition
  • 19. POTASSIUM REPLACEMENT  Do not administer potassium if serum potassium >5.5 mEq/L or patient is anuric.  Use KCl but alternate with KPO4 if there is severe phosphate depletion and patient is unable to take phosphate by mouth.  Add i.v. potassium to each liter of fluid administered unless contraindicated. Williams textbook of endocrinology 10th edition p 454 Serum K (mEq/L) Additional K required 3.5 - 4.0 - 40mEq/L 3.5–4.5 - 20mEq/L 4.5–5.5 - 10mEq/L >5.5 - Stop K infusion
  • 20. -Williams textbook of endocrinology 10th edition
  • 21.
  • 22. BICARBONATE • Clinical trials do not support the routine use of bicarbonate replacement • HCO3 replacement and rapid reversal of acidosis can impair cardiac function, reduce tissue oxygenation and promote hypokalemia and hypocalcemia. • However in presence of severe acidosis pH<6.9,in hemodynamic instability with pH<7.1 and hyperkaemia with ecg finding bicarbonate therapy considered • In the presence of severe acidosis (arterial pH <6.9), the ADA advises bicarbonate [50 mmol/L (meq/L) of sodium bicarbonate in 200 mL of sterile water with 10 meq/L KCl per hour for 2 h until the pH is >7.0]. Williams textbook of endocrinology 10th edition p456
  • 23. TREATMENT OF DKA GLUCOSE ADMINISTRATION  Plasma glucose reaches 250 mg/dl in DKA or 300 mg/dl in HHS,  Decrease the insulin infusion rate to 0.05–0.1 unit/kg/h (3–6 units/h),  Add dextrose (5–10%) to the intravenous fluids. Maintain the above glucose values until acidosis in DKA or mental obtundation and hyperosmolarity in HHS are resolved Williams textbook of endocrinology 10th edition p 455
  • 24. Criteria for resolution of DKA  glucose <200 mg/dl,  serum bicarbonate ≥18 mEq/l, and  venous pH of >7.3. Once DKA is resolved, if the patient is NPO, continue intravenous insulin and fluid replacement and supplement with subcutaneous regular insulin as needed every 4 h.
  • 25. ONCE DKA RESOLVED… • Most patients require 0.5-0.6 units/kg/day • highly insulin resistant patients – 0.8-1.0 units/kg/day • Give subcutaneous insulin at least 2 hours prior to weaning insulin infusion. Williams textbook of endocrinology 10th edition p455
  • 26.
  • 27. CLINICAL ERRORS 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 fluid when ketones still present Hypoglycemia  Insufficient glucose administration.
  • 28. Hyperglycemic-Hyperosmolar State (HHS) HNC is a syndrome characterized by impaired consciousness, sometimes accompanied by seizures, extreme dehydration, , and extreme hyperglycemia that is not accompanied by ketoacidosis.
  • 29. DKA HHS Ketonemia/Ketonuria + Ketonemia/Ketonuria - Serum Osmolality N Serum Osmolality >320mosm pH<7.3 pH>7.3 S.Glucose >250mg/dL S.Glucose >600mg/dL
  • 30. Physical examination 1. Severe dehydration is invariably present. 2. Various neurologic deficits (such as coma, transient hemiparesis, hyperreflexia, and generalized areflexia) are commonly present. Altered states of consciousness from lethargy to coma are observed. 3. Findings associated with coexisting medical problems (e.g., renal disease, cardiovascular disease) may be evident.
  • 31. Laboratory findings 1. Extreme hyperglycemia (blood glucose levels from 30 mmoll/l and over are common. 2. A markedly elevated serum osmolality is present, usually in excess of 350 mOsm/l. (Normal = 290 mOsm) 3. Serum ketones are usually not detectable, and patients are not acidic. 4. Serum sodium may be high (if severe degree of dehydration is present), normal, or high 5. Serum potassium levels may be high (secondary to the effects of hyperosmolality) Low or normal
  • 32. Treatment This condition is a medical emergency and the patient should be placed in an intensive care unit. Many of the management techniques recommended for a patient with DKA are applicable here as well. The goals of therapy include: • rehydration; • reduction of hyperglycemia; • electrolytes replacement; • investigation of precipitating factors, treatment of complications.
  • 33. Hypoglycemia It is a syndrome characterized by symptoms of sympathetic nervous system stimulation or central nervous system dysfunction that are provoked by an abnormally low plasma glucose level and it can occur at any time.
  • 34. Precipitating factors • irregular ingestion of food; • extreme activity; • alcohol ingestion; • drug interaction; • liver or renal disease; • hypopituitarism and adrenal insufficiency.
  • 35.
  • 37. Pathophysiology of hypoglycaemia Inhibition of endogenous insulin secretion Counter- regulatory hormone release • Glucagon • Adrenaline Onset of symptoms • Autonomic • Neuroglycopa enic Neurophysiologic al dysfunction • Evoked responses Widespread EEG changes Cognitive dysfunction • Inability to perform complex tasksSevere neuroglycop aenia • Reduced level of consciosn ess • Convulsio ns • Coma 83 mg/dL 58–50 mg/dL 68 mg/dL 54–43 mg/dL 54 mg/dL 50 mg/dL <27 mg/dL Arterialisedvenousbloodglucoseconcentration (mmol/L) 2. 0 3. 0 4. 0 1. 0 0 5. 0 Cryer et al. Diabetes Care 2003;26:1902–12 EEG, electroencephalogram
  • 38. Physical examination 1. The skin is cold, moist. 2. Hyperreflexia can be elicited. 3. Hypoglycemic coma is commonly associated with abnormally low body temperature 4. Patient may be unconscious.
  • 39. Treatment • The most effective treatment of an insulin reaction is the immediate ingestion of a concentrated carbohydrate source, such as sugar, honey, candy, or orange juice. • Alternative methods for increasing blood glucose may be required when the person having the reaction is unconscious or unable to swallow: – Glucagon may be given intramuscularly or subcutaneously. – In situations of severe or life-threatening hypoglycemia, it may be necessary to administer glucose intravenously.
  • 40. • BG = 40 mg%: Give (100-40) x 0.8 = 60 x 0.8= 48 ml of IV 25% Dextrose. • Repeat BG q 15 mins until BG > 70mg%. Example • If BG < 70mg% : 25% dextrose as per calculation. Check BG q15 mins • If BG > 70mg% : Check BG q30 mins till BG > 90mg% • If BG > 90mg% : Check BG q1hrly, Hold Infusion • If BG > 140mg%: Restart infusion at 50% of previous rate BG ≤70 – Suspend Insulin, Give 25% Dextrose (100-BG) X 0.8**
  • 41. Infections Complement: some studies have detected a deficiency of the C4 component in DM,this reduction of C4 is probably associated with polymorphonuclear dysfunction and reduced cytokine response Polymorphonuclear and mononuclear leukocytes: Decreased mobilization of polymorphonuclear leukocytes, chemotaxis, and phagocytic activity may occur during hyperglycemia. hyperglycemic environment inhibits glucose-6-phosphate dehydrogenase (G6PD), increasing apoptosis of polymorphonuclear leukocytes, and reducing polymorphonuclear leukocyte transmigration In tissues that do not need insulin for glucose transport, the increased intracellular glucose levels are then metabolized, using NADPH as a cofactor and the low NADPH prevents the regeneration of molecules that play a key role in antioxidant mechanisms of the cell, thereby increasing the susceptibility to oxidative stress. the glycated hemoglobin (HbA1c) is <8.0%, to maintain the proliferative function of CD4 T lymphocytes and their response to antigens.
  • 42. Infections• Respiratory infections Streptococcus pneumoniae and influenza virus • Tuberculosis • Urinary infections • Bacterial pyelonephritis E.Coli & Proteus • Emphysematous pyelonephritis E.Coli & Proteus followed by enterobacter. • Emphysematous cystitis The most frequent pathogen is E. coli, followed by Enterobacter, Proteus, Klebsiella, and Candida • Perinephric abscess gram-negative bacilli (predominantly E. coli) or polymicrobial infection • Emphysematous cholecystitis The emphysematous cholecystitis is more frequent in males with DM.The main pathogens are Salmonella enteritidis and Campylobacter • Invasive external otitis Invasive external otitis is an infection of the external auditory canal that can extend to the skull base and adjacent regions.It often affects elderly diabetic individuals and the etiologic agent is usually Pseudomonas aeruginosa
  • 43. Questions • A 39 year old Male patient presented to you in emergency department for Acute Abdomen with H/O vomiting,Restlessness,Lethargy,dehydration.On palpation of abdomen diffuse tenderness+,no guarding/rigidity.On Auscultation Bowel sounds heard. On eliciting History you detect the patient is a known diabetic and is on insulin and because of frequent travelling he is poorly complaint with insulin.Your first probable diagnosis a)Acute cholecystitis b)Perforative peritonitis c)Diabetic Ketoacidosis d)Intestinal Obstruction
  • 44. Questions • A 62 yr old Diabetic Male presented to the Emergency with H/O fever,Right Hypochondrial Pain,tachycardia for 2 days.CT abdomen done image is shown below The possible diagnosis a)Emphysematous nephritis b)Emphysematous cholecystitis c)Perforative peritonitis d)Alcoholic pancreatitis
  • 45. Questions • A 42 yr old Male known Diabetic for past 11 years with HbA1C 10.0 referred from an ENT surgeon to you the physician as a case of chronic otorrhea,otalgia with hearing loss and now presenting with facial asymmetry a provisional diagnosis of Rt. Facial N. palsy is made. You suspect an infective pathology.The Probable organism could be a)Streptococcus pneumonia b)Hemophilus influenza c)Pseudomonas aeruginosa d)Clostridium perfringens
  • 46. Questions • A 54 yr old lady who is a diabetic for 12 years brought with h/o orbital cellulitis,6th Nerve palsy and anosmia presenting with the following clinical picture the Drug of choice for this patient? a)Piperacillin Tazobactem b)Amphotericin B c)Mitomycin C d)Actinomycin D