ENDOCRINE EMERGENCIES

Dr. Diyah Saraswati, SpPD

 HYPOGLICEMIA
Unconscious Seizure
Renal failure

Sulfonilurea Palpitation

Low intake

Pallor
Sweating Weakness
 DEFINITION
 The lower limit of the fasting plasma glucose concentration is
normally approximately 70 mg/dL (3.9 mmol/L). Glucose levels
<55 mg/dL (3.0 mmol/L) with symptoms that are relieved promptly
after the glucose level is raised document hypoglycemia.
 Hypoglycemia is most convincingly documented by Whipple’s
triad:
(1) symptoms consistent with hypoglycaemia
(2) a
low plasma glucose concentration measured with a precise
method (not a glucose monitor), and
(3) relief
of those symptoms after the plasma glucose level is
raised.
ETIOLOGY
 HYPOGLICEMIA IN DIABETES
 Hypoglycemia is a fact of life for people with T1DM. An estimated 2–4% of people
with T1DM die as a result of hypoglycemia. Overall, hypoglycemia is less frequent in
T2DM.
 Relative or absolute insulin excess occurs when
(1) insulin (or insulin secretagogue) doses are excessive, ill-timed, or of the wrong
type;
(2) the influx of exogenous glucose is reduced (e.g., during an overnight fast or
following missed meals or snacks);
(3) insulin-independent glucose utilization is increased (e.g., during exercise);
(4) sensitivity to insulin is increased (e.g., with improved glycemic control, in the
middle of the night, late after exercise, or with increased fitness or weight loss);
(5) endogenous glucose production is reduced (e.g., following alcohol ingestion);
(6) insulin clearance is reduced (e.g., in renal failure).
 CLINICAL MANIFESTATION
 Neuroglycopenic symptoms of hypoglycemia are the direct result
of central nervous system (CNS) glucose deprivation.They
include behavioral changes, confusion, fatigue, seizure, loss of
consciousness, and, if hypoglycaemia is severe and prolonged,
death.
 Adrenergic symptoms such as palpitations, tremor, and anxiety
 Cholinergic symptoms such as sweating, hunger, and
paresthesias
 Common signs of hypoglycemia include diaphoresis and pallor.
 Transient focal neurologic deficits occur occasionally. Permanent
neurologic deficits are rare
 URGENT MANAGEMENT
 Oral treatment with glucose tablets or glucose- containing fluids, candy,
or food is appropriate if the patient is able and willing to take these. A
reasonable initial dose is 20 g of glucose. If the patient is unable or
unwilling, because of neuroglycopenia, to take carbohydrates orally,
parenteral therapy is necessary. IV glucose (25 g) should be given and
followed by a glucose infusion guided by serial plasma glucose
measurements. If IV therapy is not practical, SC or IM glucagon (1.0 mg
in adults) can be used, particularly in patients with T1DM.
 Because it acts by stimulating glycogenolysis, glucagon is ineffective in
glycogen-depleted individuals (e.g., those with alcohol-induced
hypoglycemia). It also stimulates insulin secretion and is therefore less
useful in T2DM.
 These treatments raise plasma glucose concentrations only transiently,
and patients should therefore be urged to eat as soon as is practical to
replete glycogen stores.
 ALGORITHM HYPOGLYCEMIA

Unconscious, suspected hypoglycemia

D40% 50 cc, IVFD D10% 500cc/8 h

 BG < 50 mg/dL, D40% 50cc

 BG < 100 mg/dL, D40% 25 cc
Glucosa monitor/15 min  BG 100-200 mg/dL, D40% (-)
 BG > 200 mg/dL, consider decreasing D10%
drip

 If BG > 100mg/dl for 3x in sequence, BG monitors/2h according protocol

above. If BG > 200mg/dl , consider to replace IVFD D10% with D5% or NaCl
 If BG > 100mg/dL for 3x in sequence, every 2h, BG monitors/4h according
protocol above. If BG > 200mg/dL, consider to replace IVFD D10% with D5% or
NaCl
 If BG > 100mg/dL for 3x in sequence, every 4h, BG monitors can be extended
as needed
 PREVENTION OF RECCURENT
HYPOGLYCEMIA
 Prevention of recurrent hypoglycemia requires an understanding of the
hypoglycemic mechanism.
o Offending drugs can be discontinued or their doses reduced.
o Underlying critical illnesses can often be treated.
o Cortisol and growth hormone can be replaced if they are deficient.
o Surgical, radiotherapeutic, or chemotherapeutic reduction of a non–β-
cell tumor can alleviate hypoglycemia even if the tumor cannot be
cured; glucocorticoid or growth hormone administration also may
reduce hypoglycemic episodes in such patients.
o Surgical resection of an insulinoma is curative;
o Partial pancreatectomy may be necessary in a nontumor β-cell
disorder.
 DIABETIC KETOACIDOSIS &
HYPERGLYCEMIA HYPEROSMOLAR STATE
Abdominal pain Naussea
Alert/stupor

Kussmaul

Inadequate Hyppotension
insulin
Vomit Keton urine

Infection

Coma Polyuria
Dehydration
PATHOGENESIS DKA AND HHS
CLINICAL MANIFESTATION DKA
CLINICAL MANIFESTATION HHS
MANIFESTATION OF
HYPERGLICEMIC HYPEROSMOLAR STATE
Altered mental states
(mental confusion, lethargy, coma)
Profound dehydration
Hypotension, tachycardia
Precipitating factor :
Infection, sepsis
Myocardial infarct, CVA
Debilitating condition (prior stroke/dementia)
Social situation
DIAGNOSTIC CRITERIA
MANAGEMENT ALGORITHM
 TRANSITION TO
SUBCUTANEUS INSULIN

 Patients with DKA and HHS should be treated with continuous

intravenous insulin until the hyperglycemic crisis is resolved.
 Criteria for resolution of ketoacidosis include a blood glucose
200 mg/dl and two of the following criteria:
o a serum bicarbonate level 15 mEq/l
o a venous pH 7.3, and
o a calculated anion gap12 mEq/l.
 Resolution of HHS is associated with normal osmolality and
regain of normal mental status. When this occurs, subcutaneous
insulin therapy can be started.
 To prevent recurrence of hyperglycemia or ketoacidosis during
the transition period to subcutaneous insulin, it is important to
allow an overlap of 1–2 h between discontinuation of intravenous
insulin and the administration of subcutaneous insulin.
 If the patient is to remain fasting/nothing by mouth, it is
preferable to continue the intravenous insulin infusion and fluid
replacement.
 Patients with known diabetes may be given insulin at the dosage
they were receiving before the onset of DKA so long as it was
controlling glucose properly.
 COMPLICATION
 Hypoglycemia and hypokalemia are two common complications with
overzealous treatment of DKA with insulin and bicarbonate, respectively,
but these complications have occurred less often with the low-dose
insulin therapy
 Cerebral edema, which occurs in 0.3–1.0% of DKA episodes in children,is
extremely rare in adult patients. Symptoms and signs of cerebral edema
are variable and include onset of headache, gradual deterioration in level
of consciousness, seizures, sphincter incontinence, pupillary changes,
papilledema, bradycardia, elevation in blood pressure, and respiratory
arrest
 PREVENTION
1) Early contact with the health care provider.
2) Emphasizing the importance of insulin during an illness and the reasons
never to discontinue without contacting the health care team.
3) Review of blood glucose goals and the use of supplemental short- or
rapidacting insulin.
4) Having medications available to suppress a fever and treat an infection.
5) Initiation of an easily digestible liquid diet containing carbohydrates and
salt when nauseated.
6) Education of family members on sick day management and record keeping
including assessing and documenting temperature, blood glucose, and
urine/blood ketone testing; insulin administration;oral intake; and weight.
 Similarly,adequate supervision and staff education in long-term facilities may
prevent many of the admissions for HHS due to dehydration among elderly
individuals who are unable to recognize or treat this evolving condition