Hyperglcemic Crises
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Transcript of Hyperglcemic Crises
DIABETIC KETOACIDOSISHYPEROSMOLAR HYPERGLYCEMIC STATE
LACTIC ACIDOSIS
HYPERGLYCEMIC CRISES
Pathogenesis of DKA
REDUCTION OF CIRCULATING INSULIN
ELEVATION OF COUNTERREGULATORYHORMONES
(glucagon, catecholamines, cortisol,growth hormone)
Pathogenesis of DKAREDUCTION OF CIRCULATING INSULIN
ELEVATION OF COUNTERREGULATORYHORMONES
↓1.increased hepatic glucose production
HYPERGLYCEMIA2. impaired glucose utilization in peripheral tissues
3.lipolysis ↑ - release of free fatty acids into the circulationand to unrestrained hepatic fatty acid oxidation to ketone bodies
(acetoacetat, β-hydroxibutyrat)↓
KETONEMIA( METABOLIC ACIDOSIS)
Hyperglycemia↓
Glycozuria↓
osmotic diuresis↓
Loss of water+electrolytes
Pathogenesis of DKA
Epidemiology
Annual incidence of DKA 0,5-0,8%Two-third of DKA patients were considered to have type1 diabetes Mortality rate 2-5%Death is rarely due to the metabolic complications ofhyperglycemia or ketoacidosis but relates to theunderlying precipitating illness.
INFECTION(30-50%)
DISCONTINUATION OF INSULIN(inadequate insulin)
NEW-ONSET TYPE 1 DIABETES
CEREBROVASCULAR ACCIDENTMYOCARDIAL INFARCTION
SEVERE TRAUMA PANCREATITIS
ALCOHOL ABUSEDRUGS
( ex.corticosteroids )
Precipitating Factors
DKA clinical picture:
The metabolic alterations typical of DKA- usually evolve within a short time frame, < 24 h.
SYMPTOMS:Polyuria, polydipsia, weight loss, weakness, Nausea,vomiting( emesis which may be
,,cofee- ground”), diffuse abdominal pain.
Polypnea;the breath has an acetone odor.Clouding of sensoria and finally coma.
DKA clinical picture:
PHYSICAL FINDINGS:Dehydration- poor skin turgor, dry mouth
Kussmaul respiration, deep, noisy pH < 7,2
Cardiovas.- Tachycardia; Hypotension or normal BP;
Neuro. – mental status can vary from full alertness to profound lethargy or coma
Hypotermia ( peripheral vasodilation );
LABORATORY FINDINGS
Glucose(mg/dl)PH –
Bicarbonate(mEq/l) Osmolality
Ketonemia/Ketonuria Na(mEq/l), K(mEq/l)
Anion gap = [Na+] - [Cl- + HCO3-]
BUN, creatinine,complete blood count, ECG, chest X-ray
Urine or blood cultures,etc.
DKA....Laboratory
Hyperglycemia is a key diagnostic criterion of DKA, however, a wide range of plasma glucose can be present on admision.
~10% of DKA presents glucose levels≤ 250mg/dl due to antecedent food restriction, inhibition of gluconeogenesis or insulin injection en route to the hospital.
Leukocytosis (10000-15000mm³) is the rule in DKA and may not be indicative of an infectious process.
DKA....Laboratory
Hyperamylasemia has been reported but there is little correlation with the presence of gastrointestinal symptoms
Na+ = ↑ N or ↓ ( usually low because of the osmotic flux of water from intracellular to extracellular space)
K+ = , N or ( usually elevated because of an extracellular shift of potassium caused by acidemia )
DKA....Laboratory
Accumulation of ketoacids results in pH ˂7,30and an increased anion gap metabolic acidosisDKA intensity – pH, HCO3
-
AG = [Na+] - [Cl- + HCO3-] AG > 10-12 mmol/l indicate the
presence of increased anion gap metabolic acidosis.
Severe DKA AG = 25 – 35mmol/lKetonuria – not correlate with the intensity of acidosis
Diagnostic criteria for DKA
MILDEMILDE MODERAT MODERATEE SEVER SEVEREE Plasma glucosePlasma glucose >250 mg/dl >250 mg/dl >250 >250 mg/dl >250 mg/dl >250 mg/dlmg/dl
AArterial rterial pHpH 7,25-7,3 7,25-7,300 7-7,25 < 7 7-7,25 < 7
SerumSerumHCOHCO33--(mEq/i) 15-18 10-15 < 10(mEq/i) 15-18 10-15 < 10
Urine ketone Urine ketone pozitiv pozitivee pozitiv pozitivee pozitiv pozitiveeSerum ketone Serum ketone pozitiv pozitivee pozitiv pozitivee poziti pozitieeii
Serum osmolalitySerum osmolality. variab. variablele variab variablele variab variablele
AAnionnion gap gap >10 >12 >12 >10 >12 >12
Mental sMental status tatus alertalert alert/drowsyalert/drowsy stupor/comastupor/coma
ALCOHOLIC KETOACIDOSIS
STARVATION KETOSIS
Other METABOLIC ACIDOSIS(lactic acidosis, ingestion of salicylate ,methanol,ethylenglycol,paraldehyde)
GASTROINTESTINAL SYMPTOMS(ex. serum lipase determination may be beneficial in the dif.diag.of pancreatitis)
COMA
DIFFERENTIAL DIAGNOSIS
Corection of:
Dehydration
Hyperglycemia
Electrolyte imbalances
± use of bicarbonate
Treatment of comorbid precipitating events
TREATMENT OF DKA
Frequent patient monitoring !!!!
2 h. control glycemia electrolytes
physical examination
Fluid therapy
Isotonic saline (0,9% NaCl) is infused at a rate of 15-20 ml/kc body w./h or 1l during first hour
Subsequent choice for fluid replacement depends on hemodynamics,the state of hydration, serum electrolyte levels and urinary output.
5% dextrose should be added when plasma glucose is ≤ 250 mg/dl.
!!! REGULAR INSULIN !!!
The administration of continuous intravenous infusion of regular insulin is the preferred route
↓
Treatment algorithms recommended the adm. of an initial intravenous dose of regular insulin
0,1u/kgCfollowed by the infusion of 0,1u/kg/h
If serum glucose does not fall by 10% in first hour(50- 70mg/dl/h) the insulin infusion shoud be increased
every hour.
INSULIN therapy
POTASSIUM < 3,3 mEq/l → + 40 mEq K ≥3,3 – 5 mEq/l → + 20-30 mEq K
≥ 5,0 mEq/l → NO
Insulin therapy,correction of acidosis and volume expansiondecrease serum potassium concentration!
To prevent hypokalemia, potassium replacement is initiated after serum levels fall below 5mEq/l
ELECTROLYTE replacement
PH < 6,9 NaHCO3 – 100 mmol in 400ml steril water
PH > 7,0 No
BICARBONATE therapy
HYPOPOTASEMIA
HYPOGLYCEMIAare two common complications
CEREBRAL EDEMA prevention might include
avoidance of excessive hydration anda gradual decrease in serum glucose
PULMONARY EDEMA HYPERCHLOREMIC ACIDOSIS
DEATH
COMPLICATIONS
PREVENTION
Many cases of DKA and HHS can be prevented by :
better access to medical care,proper patient education, andeffective communication with a health care providerduring an intercurent illness.
HYPEROSMOLAR HYPERGLICEMIC STATE
Definition:Hyperosmolarity(Osm > 320-330 mosm/kg) Hyperglycemia Dehydration Occurs in middle-aged and older adults with
type 2 diabetes In most patients with HHS, restricted water intake is
due to patient being bedridden and is exacerbated by the altered thirst response of the elderly.
Ketonuria and acidosis are missing!Ketonuria and acidosis are missing!
Hyperglycemia↓
Glycozuria↓
osmotic diuresis↓
Loss of water+electrolytes
Pathogenesis of DKA
Pathogenesis of HHS
Insulin levels in HHS are inadequate to facilitate glucose utilization by insulinsensitive tissues but adequate to prevent lipolysis and subsequent ketogenesis!
HHS clinical picture:
The process of HHS usually evolves over several days to week !
intense thirstpolyuriaweaknessmental status can vary but coma is more frequent.± focal neurologic signs(hemianopsia, hemiparesis)
and seizures(focal or generalized) may also be features of HHS (exam. CT)
HHS clinical picture:
Physical examination
Severe dehydration (hypoT, tahycardia ± shock)stupor / comaOliguria suggests Acute renal failure due to
dehydration (prerenal azotemia or preexisting chronic renal failure)
DIAGNOSIS
Precipitating Factors
Infection- particulary pneumonia or gram-negative sepsis, is the most common initiating event.
Myocardial infarction, cerebrovascular accident, TE, Pancreatitis
Burns / Severe traumaDrugs diuretics - enhances dehydration, corticosteroids PhenytoinAntipsychotic drugs
HHS....Laboratory
Severe hyperglycemia (800….2400 mg/dl)Hyperosmolarity - (320 -440 mOsm/kg) Na+ = , N or ↑↑Osm pl = 2 x (Na +glu / 18) N = 290-310 mOsm/kg
Treatment of HHS
COMPLICATIONS / PrognosticRhabdomyolysis(non-traumatic.)
CreatinKinase (> 1000U/l) One of the dreaded complications of R. is Kidney failure. Pulmonary thromboembolism;Peripheral venous thrombosis- Mortality attributed to HHS is considerably higher than
that attributed to DKA(˃10 times)- The prognostic is substantially worsend at the
extremes of age in the presence of coma, hypotension and severe comorbidities.
Lactic Acidosis
LA may develop in any state of:1. Diminished tissue oxygenation(eg.vascular shock)-
excessive lactat production. 2. Hepatic dysfunction (and diminished conversion of lactat
to glucose)LA is characterized by low pH acompanied by the buildup of
lactat.
Abnormal anion gap + Lactat level > 7 mmol/l
Causes of LA
ShockSepsisEthanol toxicityHepatic diseaseDiabetic ketoacidosisDrugs: metformin/ phenforminInborn error of metabolism
Symptoms
Nousea, vomiting, abdominal painHyperventilation (to remove CO2)Severe anemiaHypotension Irregular heart rateTachycardia Anxiety/ lethargy
Treatment of LA
1.Sodium bicarbonat administration !2.The primary condition underlying the acidosis should
be corrected.3. ± hemodialysis.
References
Abbas E. et.al Hyperglycemic Crises in Adult Patiens withDiabetes/ADA Statements. Diabetes Care,vol.32(7),july 2009Joslin”s Diabetes Mellitus 13th Edition, edited byC.Ronald Kahn, Gordon C.Weir