SGD Case 7: Hyperosmolar Hyperglycemic State

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OS 212: Reproduction & Hormone Control: ENDO
Dr. Sison
SGD Case 7: Hyperosmolar Hyperglycemic State
Also see section on differentials
After Hx & PE, the Patient:
♪
Is hypotensive, tachycardic, tachypneic, febrile
♪
Is manifesting dehydration (a symptom)
♪
May have an infection (specifically UTI, from the
suprapubic tenderness)
I. History and PE
History:
FR, a 72 year old female, has a strong family history of diabetes
but she was never under medical care as there was no doctor in
their barangay. The family claims that she was previously well and
asymptomatic. One week prior to consult, she had decreased
appetite and fever but continued with her usual daily activities.
She did not seek consult nor take any medications. 3 days prior,
she was lethargic and would prefer to stay in bed the whole day.
This prompted relatives to bring her to the hospital.
Physical Examination:
General Survey
Drowsy, disoriented to time and place,
weak-looking
Vital Signs
BP: 90/60
HR: 110
Temp: 37.9 C
RR: 22
Skin/Mucosa
Anicteric sclerae, pink conjunctivae,
dry oral mucosa, sunken eyeballs
Chest and Lungs Equal chest expansion, clear breath
sounds, no crackles, no axillary sweat
Abdomen
Scaphoid abdomen, normoactive
bowel sounds, no tenderness
Extremities
Pink nailbeds, no pathologic reflexes
and neurologic deficits
Maam says: Impression from Hx & PE, Differentials from Hx, PE &
Labs.
III. Lab Results
Blood:
Parameter
CBG: 729 mg/dL
Creatinine: 201 umol/L
BUN: 30.7 mg/dL
Sodium: 148 mmol/L
Potassium: 3.9 mmol/L
♪
Interpretation
High
High
High
High Borderline
Normal
In the setting of hyperglycemia, hyponatremia is common
due to the osmotic effect of glucose drawing water into the
vascular space; therefore, in HHS suspects it is important to
compute for the value of Na in the absence of hyperglycemia
(Corrected Serum Sodium) using the following formula:
1.65 (mg/dL glucose 100)
100
*correct serum Na only when glucose >200 mg/dL
Corrected
Serum Na
=
Na
(mmol/L)
+
148 meq/L + 1.65 (729-100)
100
= 158.4 meq/L High
Cranial Nerve Examination:
Effective Sodium Osmolality:
Pupils 2-3 mm EBRTL
Full EOM’s
No ptosis
Intact facial sensation V1-V3, bilateral
No facial asymmetry
Intact gross hearing
Uvula midline
Good shoulder shrug, Tongue midline
Effective
Osmolality
=
2[measured
Na
(meq/L)]
+
glucose (mg/dl)
18
=(2 x 158.4 mEq/L) + 729 mg/dL
18
= 357.26 mOsm/kg H2O  High (N: 270-300)
Pertinent Findings:
1. Marked hyperglycemia
2. Hypernatremia
3. Increase BUN and Creatinine consistent with HHS – signs of
acute renal failure (ARF)
4. BUN/Creatinine Ratio (13.5) supports Acute Renal Failure
secondary to dehydration (prerenal ARF) – there are specific
values set to determine the level of renal failure
☼ If <10 due to intrinsic renal failure
☼ 10-15 due to oliguric acute renal failure
☼ If >20 due to dehydration (prerenal azotemia)
5. Hyperosmolarity
No preferential movement of the extremities
Intact sensation in all extremities
DTR ++ on all
Supple neck
--------------
Pertinent in History
♪ strong family hx of diabetes
♪ no previous intake of medicines
♪ previously well and asymptomatic
♪ 1 wk PTC: decreased appetite, fever
♪ 3 days PTC: lethargic
Pertinent in PE
♪ Drowsy, disoriented, weak-looking
♪ BP 90/60, HR 110, RR 22, Temp 37.9 °C
♪
♪
Normal
>200mg/dl
53-115 umol/L
8 – 25 mg/dL
135-145mmol/L
2.8-6.7 mmol/L
Corrected Serum Sodium:
Neuro Exam: essentially normal
☼
1
II. Initial Impression
OUTLINE (~5 qtns from this trans)
I.
History & PE
II.
Initial Impression
III.
Lab Results
IV.
Differential Diagnoses
V.
Pathophysiology Of HHS
VI.
Management
♪
EXAM
Meme says: Hypotensiontachycardia (compensation)
Dry oral mucosa, sunken eyeballs, dry axilla, and poor
skin turgor
(+) suprapubic tenderness
Normal neurologic exam
Page 1 of 5
THURSDAY | 10月 08日 2009年
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OS 212: Reproduction & Hormone Control: ENDO
SGD Case 7: Hyperosmolar Hyperglycemic State
Urinalysis:
SEPSIS
Parameter
Specific gravity: 1.030
Epithelial cell: rare
RBC: 3 – 4
WBC: too numerous to count
Casts: none
Ketones: negative
Normal
1.005-1.025
Few
0-3hpf
0-4hpf
Negative
Negative
Interpretation
High
Normal
High
High
Normal
Normal
Pertinent Findings:
1. High WBC count suggests lower UTI
2. Specific gravity is high, suggesting prerenal ARF (>1.020)
SUBSTANCE TOXICITY
DIABETIC KETOACIDOSIS (DKA)
Arterial Blood Gas:
Parameter
pH : 7.41
pCO2: 38
pO2 : 105
HCO3 : 23.5
O2 sat: 99%
Normal
7.3 – 7.45
32 – 45
70 – 104
22 – 26
94% – 100%
Interpretation
Normal
Normal
High Borderline
Normal
Normal
♪
How to interpret an ABG result:
1. Interpret if pH is acidic or alkalinic (below/above 7.4)
2. Determine if pCo2 and pO2 follows the trend  primary
problem
3. If they do not concur (as in the case above), determine
which (1 or 2) has a greater magnitude from the normal.
♪
Meme says:
☼ If increased pH & pCO2>45Primary Pulmonary alkalosis
☼ If increased pH & HCO3 >30 Primary Metabolic Alkalosis
♪
Maam says: I don’t like this lab test result.
Other serum electrolytes
CBC
HbA1c
Serum ketones
Urine culture
Brain CT scan
KUB Utz
HHS
ADDISON’S
DISEASE
adrenal glands do not
produce enough of the
hormone cortisol and, in
some cases, the hormone
aldosterone
(adrenal
disorder1’ or defective
ACTH
secretion
by
pituitary2’)
DEMENTIA - progressive
decline
in
cognitive
function due to damage or
disease in the body beyond
what might be expected
from normal aging
Fever,
Tachycardia
Tachypnea, UTI
(urinalysis
&
suprapubic
tenderness),
encepalopathy
Tachycardia
Dehydration
Lethargy
Tachycardia
Dehydration
Can present
similar to HHS
Lethargy
1
Px has this
Diagnostics: inc WBC
Px has this
Diagnostics: Inc BUN
and Creatinine, Inc
Spec. Gravity
No Hx of substance
abuse, alcohol intake,
cigarette smoking
No Kussmaul’s
breathing, nausea,
vomiting, abdominal
tenderness and
ketone breath
Diagnostics: CBG> 700
mg/dl not indicative of
DKA, (-) ketones on
Urinalysis
Increased Glu
(If Px has normal
Glucose levels,
request for Thyroid
hormone levels)
V. Pathophysiology of HHS
ARE YOU CRAMMING? THEN LOOK AT THE APPENDIX FOR A
PATHOPHYSIO-FINDING FLOWCHART.
HALLMARKS OF HHS
1. Marked hyperglycemia
2. Marked hyperosmolarity
3. Mild or absent ketonemia
IV. Differential Diagnoses
DIFFERENTIAL
DIABETES MELLITUS II
HYPOTHYROIDISM
EXAM
It is a relatively common life threatening endocrine
emergence that is reported in all age groups but more frequently
affects older patients with Type 2 DM.
Other Diagnostic Tests:







ACUTE RENAL FAILURE
Dr. Sison
RULE IN
Family Hx, high
CBG
Lethargy,
hypotension,
dehydration,
tachycardia,
abdominal
tenderness
Lethargy
Dehydration
RULE OUT
Px has this
Diagnostics: high CBG
Can’t be ruled out due
to high CBG &
Dehydration
Hyperosmolar hyperglycemic state and diabetic
ketoacidosis may represent opposite ends of the spectrum of
decompensated diabetes that differ in the time of onset,
degree of dehydration, and the severity of ketosis.
The mortality rate of hyperosmolar hyperglycemic
state ranges from 10 to 50 percent, a considerably higher rate
than that of diabetic ketoacidosis (1.2 to 9 percent).
Meme says:
* HHS = Insulin deficiency + Inadequate fluid
hypoglycemia
hyponatremia
hyperpigmentation
no abdominal pain
no diarrhea
♪
♪
♪
Lethargy,
Can cause
malnutrition
and
dehydration
Insulin deficiencydecreased Glu uptakeweakness
Hyperglycemia (from dec. Glu uptake) excess Glu in
urineosmotic
dieresisintravascular
volume
depletion
intravascular volume depletion + inadequate fluid
replacement = dehydration
No aphasia, apraxia,
agnosia or abnormal
executive
function;
Maam says: should be
the last on list, cannot
rule out (but in this
case obvious naman
daw na may organic
problem)
Page 2 of 5
THURSDAY | 10月 08日 2009年
AL__in!
OS 212: Reproduction & Hormone Control: ENDO
SGD Case 7: Hyperosmolar Hyperglycemic State
Table. Common Lab Results of HSS as compared with DKA
Dr. Sison
EXAM
1
and increasing hepatic glucose production. This leads to
hyperglycemia, resulting in glycosuria and osmotic
diuresis with obligatory water loss, leading to
intravascular volume depletion which is further
exacerbated by inadequate fluid intake.
From 2011 Trans
NOTES on Pathophysiology:
1. If the patient is an uncontrolled hypertensive, the blood
pressure may still appear normal on physical examination
(relative hypotension) even if the patient is already
severely dehydrated.
2. It should be emphasized that HHS causes intracellular
dehydration as opposed to other causes of dehydration.
Typical Manifestations of HHS
♪ The prototypical HHS patient is an elderly individual
with a Type 2 DM.
♪ Several week history of polyuria and weight loss
♪ Altered Mental Status: lethargy, confusion, coma
♪ Severe Dehydration: dermal & mucosal changes,
weight loss, hypotension
♪ Motor abnormalities: fasciculation, tremors, focal
motor seizures
♪ Meningeal signs
☼ Kernig’s Sign: bilateral pain and increased
resistance to extending the knee
☼ Brudzinski’s Sign: flexion of hips and knees as
the neck is flexed
Remember that for HHS to develop, you need to have:
♪ Reduction in effective insulin Function
♪ Increase in counterregulatory Hormones
stress(infections etc.)INC in Cortisol, glucagon
etc.INC in blood sugarRELATIVE insulin deficiency
♪ Increase in hepatic, renal glucose production
♪ Impaired glucose utilization in peripheral
tissuesHYPERGLYCEMIA
♪ Change in osmolality of Extracellular Space
♪
Lethargy and confusion
☼ The decrease in plasma volume due to dehydration
causes renal insufficiency. Decreased intravascular
volume decreases glomerular filtration rate. Renal
glucose excretion is limited and contributes to the rise
in serum glucose. The loss of more water than sodium,
with the concomitant increase in glucose level, leads to
hyperosmolarity. Hyperosmolarity causes water to be
drawn out of cerebral neurons, resulting in mental
obtundation.
☼ The degree of neurologic impairment is related directly
to the effective serum osmolarity.
♪
Elevated creatinine, BUN
☼ Creatinine, blood urea nitrogen (BUN), and hematocrit
levels are almost always elevated. HHS produces
significant total body losses of many electrolytes.
♪
Negative for ketones
☼ The absence of ketosis in HHS is not completely
understood. Presumably, the insulin deficiency is only
relative and less severe than in DKA, and it is believed
that the presence of even small amounts of insulin can
prevent the development of ketosis by inhibiting
lipolysis in the adipose stores. Even with a low
insulin:glucagon ratio, which promotes hepatic
ketogenesis, the limited availability of precursor free
fatty acids from the periphery restricts the rate at which
ketones are formed.
☼ It is also possible that the liver is less capable of ketone
body synthesis or that the insulin/glucagon ratio does
not favor ketogenesis.
Precipitating Factors for HHS
1. Infections
2. Medications
3. Non Compliance
4. Undiagnosed Diabetes
5. Substance Abuse
6. Coexisting Disease
Table. Common Precipitating Factors
Correlation of Findings with Pathophysiology of HHS
♪
72 year old female; no known medical problems
☼ Typically, patients presenting with HHS are older and
have undiagnosed diabetes. Undiagnosed diabetes
often is HHS because of failure to recognize early
symptoms of the disease.
♪
Fever; WBC in urine
☼ Infection, Sepsis
☼ Sepsis, pneumonia and other serious infections are
frequent precipitants of HHNS.
♪
Dry oral mucosa, poor skin turgor, sunken eyeballs, no
axillary sweat, hypotension, tachycardia  manifestations
of dehydration
☼ Insulin deficiency reduces glucose utilization by muscle,
fat and the liver, while inducing an increase in glucagon
Page 3 of 5
THURSDAY | 10月 08日 2009年
AL__in!
OS 212: Reproduction & Hormone Control: ENDO
SGD Case 7: Hyperosmolar Hyperglycemic State
Dr. Sison
EXAM
1
VI. Management
HHS is a diabetic emergency! As with any other emergency,
maintain Airway, Breathing, and Circulation before starting any
form of intervention. This entails preparing for intubation if the
patient goes into coma, giving O2 as necessary and cautious
administration of IV fluids to prevent inducing an MI or CVA.
According to American Diabetic Association,
These are the 5 pronged approach to HHS:
♪ Vigorous intravenous rehydration
♪ Electrolyte replacement
♪ Administration of intravenous insulin
♪ Diagnosis and management of precipitating and coexisting problems
♪ Prevention
RISA|リサ|Shucks ang hirap mag-compile at lay-out ng trans-from-scratch
ng may dysme! Huhu… Gerald, magsisimula ka na ba ng illegal business?
Di ka pa ata nahahawaan ni Ivan, na hinawaan ako ng sipon. Maui at
Cybill, magkakaroon din kayo ng bacterial conjunctivitis sa Sem break.
Wahahaha. Kitel, TRP na! Nico, belated happy birthday sa inyo ni Reg,
salamat pala ulit sa feeding frogram. Alex, kahit taon-taon, tutugtugan
kita, gagandahan ko pa every year. Ces, say o na baonan ko. AJ, salamat,
bigay ko pala CD next week. And to take a leaf from Daniel D.’s book:
Hello skating rink. Nakapag-trans na ulit ako, di pa rin tayo nagkikita.
10 rules on dating my sassy girl
Management:
♪ Antibiotics (broad-spectrum) for the UTI
♪ Monitor: urine output, serum electrolytes, sensorium,
blood sugar, VITAL SIGNS
1. First, don't ask her to be feminine.
2. Second, don't let her drink more than 3 glasses. She'll beat someone.
3. At a cafe, drink coffee instead of coke or juice.
4. If she hits you, act like it hurts. If it hurts, act like it doesn't.
5. On your 100th day together, give her a rose during her class. She'll like it a lot.
6. Make sure you learn fencing and squash.
7. Also, be prepared to go to prison sometimes.
8. If she says she'll kill you, don't take it lightly. You'll feel better.
9. If her feet hurts, exchange shoes with her.
10. Finally, she likes to write. Encourage her.
Principles of Management
♪ Fluids: 15 to 20 mL / Kg / hr of normal saline - depends
also on the cardiac status of the patient (elderly
individuals must be monitored for pulmonary
congestion)
☼ 0.9 NSS for hypotensive Px
☼ ½ 0.9 NSS for normotensive Px
♪
♪
Insulin Therapy: regular insulin 0.15 unit/ kg IV bolus,
then regular insulin 0.1 unit/kg/hr IV infusion
☼ In contrast to DKA, HHS patients must not have
subcutaneous insulin since they are frankly
hypotensive and perfusion is compromised and
there is a risk for delay in the absorption which
should not be the case (emergency!);
☼ IV for HHS!!!
Electrolytes
☼ Watch out for POTASSIUM
 Hypokalemic, normal state
 hydration + insulin (during mgt.)
 intracellular influx of Potassium
 possible aggravation of hypokalemia
☼
Hypomagnesemia – also monitor Mg levels since
Mg derangements preclude correction of
hypokalemia
Complications of Management
♪ Hypoglycemia
♪ Hypokalemia (most fetal consequence: cardiac
arrhythmias; presents initially as weakness or paralysis)
♪ Hypernatremiadue to aggressive infusion of IV
isotonic solution (mental status is altered; inc risk for
morbidity)
♪ Cerebral edema (mannitol should be administered! Call
neuro department)
♪ Vascular occlusions
♪ Rhabdomyolysis
♪ ARDS
♪ Cerebral Edema
Maam says: If the Px does not wake up even if fluids, electrolytes
and insulin were administered, then consider a neurological or
thyroid problem.
Para sa Block B na di nakabasa:
"Dalawampung Hakbang sa Dambana"
Isa... Dalawa… Tatlo...
Alam kong gasgas na ang linyang ito pero anu’t ano pa, hayaan mong sabihin kong walang anumang
salita mula sa kahit ano pang lenguahe ang magbibigay kahulugan sa pakiramdam ko ngayon.
Ikakasal ka na.
Mula sa kinalalagyan ko, habang dahan dahan mong binabaybay ang gitna ng simbahan, hindi ko
mapigilang lumuha ng maliliit na patak.
Ikaw ba talaga yan? Makailang pikit na ang ginawa ko, tinatanong ang sarili kung ikaw nga ba ang
babaing nasa traje de boda. At kahit anong pikit ang gawin ko, ikaw nga iyon.
Parang kailan lang, kalaro kita kasama ang ibang bata. Alam ko pa ang itsura mo noon; tisay pero
bulok ang ipin, naka-ponytail ka na palagi noon pa, at chubby. Bibo kang kalaro sa piko, pero kapag
pikon ka na sa pang-aasar nila dahil sa lagi kang natutumba pag isang paa na lang ang gamit sa
number 3 o kaya 4 na box sa piko, sa akin ka iiyak at aawayin ko sila. Madalas nila tayo tuksuhin
pero wala lang sa iyo yon. Natutuwa naman ako noon dahil sa akin ka lumalapit. Para sa akin, ikaw
na ang bestfriend ko.
Apat… Lima... Anim…
Binibilang ko ang mga hakbang mo sa altar. Ilang segundo na lang ay hindi ka na single. Masaya ka
kaya habang naglalakad? May luha ka din sa mata, nakikita ko. Pero ang tanong na bumabalot sa
isip ko ay kung luha ba yan ng kagalakan o kalungkutan.
Hindi kita naging kaklase sa grade school. Palibhasa palagi kang nasa star section. Sa service lang
kita nakakasabay, at habang kumakain tayo ng cotton candy ay nagkukuwentuhan tayo tungkol sa
mga nangyari sa araw natin sa school. At alam ko, nalulungkot ka noon kapag bababa na ako sa
bahay namin. Magba-bye ako sayo habang aandar ang service at magtititigan tayo. Close tayo
noong elementary. Ako ang bestfriend mong lalaki at ikaw naman ang tangi kong bestfriend na
babae.
Pito... Walo... Siyam…
Mahal na mahal kita. At habang pinagmamasdan kita sa maganda mong gown ay parang
natutunaw ako sa kinalalagyan ko. Nasa kalagitnaan ka na at maya maya pa ay magsisimula na ang
seremonya.
Nag-high school tayo sa parehong school at sa kabutihang palad ay ka-section kita. Lalo pa tayong
naging close kahit pa parating magkaaway ang mga barkada mong babae at ang mga barkada kong
lalaki. Pero di gaya noong mga bata pa tayo, sa iba ka na tinutukso.
End of IT
Page 4 of 5
THURSDAY | 10月 08日 2009年
AL__in!
OS 212: Reproduction & Hormone Control: ENDO
SGD Case 7: Hyperosmolar Hyperglycemic State
Dr. Sison
EXAM
1
APPENDIX
Sampu… Labing-isa… Labing-dalawa…
Pakiramdam ko, palakas nang palakas ang tugtog ng kasal habang papalapit ka sa altar.
Nakangiti ka at kung minsa’y naititingin mo ang mata mo sa ibang taong nagagalak
habang pinagmamasdan ka. Nasa sa iyo lahat ng atensyon.
Nagkaroon ka na ng maraming boyfriend. Ako namam ay umasa lamang na maibig mo.
Wala akong naging ibang inalayan ng pagmamahal kundi ikaw. At tuwing pinapaiyak ka
ng mga magagaling mong ex, telepono ko ang kumikiriring. Kaya nga noong nauso ang
kantang “Halaga” ng Parokya ni Edgar, ay sobrang tinamaan ako.
Labing-tatlo… Labing-apat… Labing-lima…
Maligaya ka sa panahong to, alam ko. Ikaw pa, kilalang kilala na kita. Bestfriend kita eh.
Mula ulo hanggang paa, kilala kita. Kakatawa pero naaalala ko pa noong mga bata tayo,
alam ko na ang mga panty mo ay yung may burdang Monday, Tuesday, hanggang Friday.
Alam ko na noong elementary ay galit ka sa Sibika at Kultura at sa Principal nating
tinawag nating Miss Minchin. Noong highschool, alam ko pa kung sinu-sino ang mga
naging crush mo. Kabisado na kita. Alam ko kung mainit ang ulo mo, kung malungkot ka,
kung hindi maganda ang pakiramdam, kung nae-excite at lahat lahat.
Alam ko din kung maligaya ka. At kung hindi man ako nagkakamali, nararamdaman kong
masaya ka ngayon habang patungo sa altar.
Labing-anim… Labing-pito… Labing walo…
Basta maligaya ka, masaya ako. Yun naman ang gusto ko parati, ang
maligaya ka. At ang tanging hiling ko sa panahong ito ay ang panghabambuhay mo nang kaligayahan.
Ayan na malapit ka na sa altar.
Labing-siyam…
Eksaktong ikalabing-siyam na ang ang hakbang mo, nabilang ko sa isip.
Congratulations. Masaya ako at alam kong masaya ka rin ngayong ikakasal
ka na…
Dalawampu…
… sa akin.
ULY: I love you Chekai!
Quota!
Page 5 of 5
THURSDAY | 10月 08日 2009年
AL__in!
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