29 year old female presents abdominal pain, nausea, vomiting, and confusion. Patient stated her nausea and abdominal discomfort began a few days ago and has progressively gotten worse. She states she is a diabetic and her sugars have been running high. She explains she was supposed to switch insulin regimens a week ago, but had some issues at the pharmacy and has continued on her previous regimen until those issues are resolved. She was diagnosed with diabetes 5 years ago following her first pregnancy in which she had gestational diabetes.
Weight: 80kg
PMH: Diabetes
Allergies: NKDA
Meds: 20 units NPH qd, NovoLog 13 units with meals, Prenatal Vitamin
VS: BP 110/70, HR 106, T99, RR16
PE:
CV: normal S1, S2, no MRG, 2+ peripheral pulses, no cyanois, cap refill < 2 secs
Pulm: lungs CTAB, normal work of breathing
Abdomen: soft, non-distended, mild tenderness to palpation, bowel sounds normative x 4
Neuro: mild confusion, appropriate deep tendon reflexes, cranial nerves intact
Skin: supple, moist, no rashes, ulcers, or lesions
HEENT: normocephalic atraumatic, nasal mucosa moist, nares patent, oropharynx pink and moist without erythema or exudate, trachea midline, no lymphadenopathy
Labs:
Hb: 12
Hct: 38
WBC: 14
Plt: 152
Na: 140
K: 3.5
Cl: 100
CO2: 28
BUN: 18
Cr: 0.9
Glu: 442
Serum Osm: 330
UA: negative (no WBC, no RBC, no Ketones, etc.)
Urine HCG: negative
Tests / Imaging:
KUB: no acute findings
CXR: no acute findings
EKG: sinus tachycardia
1. What is your differential diagnosis? (Will list some follow up questions about making a plan)
Weight: 80kg
PMH: Diabetes
Allergies: NKDA
Meds: 20 units NPH qd, NovoLog 13 units with meals, Prenatal Vitamin
VS: BP 110/70, HR 106, T99, RR16
PE:
CV: normal S1, S2, no MRG, 2+ peripheral pulses, no cyanois, cap refill < 2 secs
Pulm: lungs CTAB, normal work of breathing
Abdomen: soft, non-distended, mild tenderness to palpation, bowel sounds normative x 4
Neuro: mild confusion, appropriate deep tendon reflexes, cranial nerves intact
Skin: supple, moist, no rashes, ulcers, or lesions
HEENT: normocephalic atraumatic, nasal mucosa moist, nares patent, oropharynx pink and moist without erythema or exudate, trachea midline, no lymphadenopathy
Labs:
Hb: 12
Hct: 38
WBC: 14
Plt: 152
Na: 140
K: 3.5
Cl: 100
CO2: 28
BUN: 18
Cr: 0.9
Glu: 442
Serum Osm: 330
UA: negative (no WBC, no RBC, no Ketones, etc.)
Urine HCG: negative
Tests / Imaging:
KUB: no acute findings
CXR: no acute findings
EKG: sinus tachycardia
1. What is your differential diagnosis? (Will list some follow up questions about making a plan)
DKA
ReplyDeleteIf you'd like to pursue the diagnosis of DKA, what other tests would you want ordered to confirm your suspicion?
ReplyDeleteAlso, what other diagnoses might be in your differential?
diabetic hyperosmolar syndrome
ReplyDeleteWhat is that?
DeleteLook up HHS (hyperosmolar hyperglycemic state)
DeleteGotcha..actually it was talked about today ironically! Totally forgot about that one! Thanks for doing this Aaron!
DeleteThis comment has been removed by the author.
ReplyDeleteABG Results:
DeletePH: 7.35
PO2: 89
PCO2: 40
HCO3: 28
This comment has been removed by the author.
ReplyDeletewouldn't a lack of ketones in the urine rule out DKA?
ReplyDeleteNot just the lack of ketones, but this patient also lacks a truly acidotic state. Their pH is ok and their bicarb is normal.
DeleteThis patient has HHS (hyperosmolar hyperglycemic state).
Now that we know the diagnosis, what is your plan? Also, what are the most lethal complications of HHS and what are some causes of HHS?
well i know that patients with HHS are also dehydrated causing the tachycardia so i would assume insulin for the hyperglycemia and fluids to correct the dehydration
Deleteyou would also be concerned about hypokalemia, right? due to giving the patient fluids.. it can make the body uptake more K+ in the body
DeleteI agree with HHS, but did we also get a pregnancy test? Cant a DM pt have a hyperglycemic episode during pregnancy considering she is having issues with her previous insulin too?
ReplyDeleteonce again I didn't see the HCG test was negative.. lol I'm one step behind. I am still curious if just being pregnant could cause an HHS episode though.
DeleteThe urine HCG was negative. Good thinking, though. Any woman with a uterus and abdominal pain gets a urine HCG.
ReplyDeletecould pregnancy cause the patient to go into HHS?
DeleteLots of good questions.
ReplyDeleteIn regards to hypokalemia: you can get some fluid overload leading to electrolyte abnormalities, but the greater risk in this case is causing hypokalemia by administering insulin. Insulin drives potassium back into cells which would drop the amount of potassium in the bloodstream. In the situations of HHS or DKA you only initiate insulin if K > 3.3 (so in this case you could start it, however; insulin management in these cases must be carefully titrated and many parameters must be monitored)
There are many things that can cause a diabetic to go into DKA or HHS. Essentially anything that increases stress on the body, one of which could be pregnancy. However; this is not one of the most common causes of DKA or HHS.
So, new questions:
- What are the most common causes of hyperglycemic states?
- What type of diabetics are more likely to get DKA over HHS?
We'll try to wrap this case up sometime tomorrow with a few key points and the reasoning behind choosing this case.
Type I Diabetics are much more likely to have DKA than Type II diabetics. A common cause for becoming hyperglycemic would be illness of some kind (stress on the body). I think maybe eating too many carbs and not taking enough insulin and noncompliance of meds would be common too but not sure on those.
DeleteDKA- I'd say most due to:
Delete1. Infection of any kind(esp. sepsis)
2. Missing insulin doses
3. Initial onset of Diabeetus
Seems like DM1's would be likely to get DKA and DM2's more likely to get HHS. That's just a general rule from what I remember. Ketones +/- would be the differentiation I think. Treatment would be very similar/same and differentiating the two would not seem to matter unless the pt was a new diabetic.
So yeah, pretty much what Carleigh said...
Dx: Hyperosmolar Hyperglycemic State
ReplyDeletePertinent Positives: elevated glucose, elevated serum osmolality, neurological symptoms, insidious onset, type 2 diabetic
Pertinent Negatives: no acidosis, no urine ketones, normal serum bicarbonate
Common precipitating factors: infection (most often pulmonary or urinary), inadequate insulin therapy. In this case the patient was clearly on inadequate insulin therapy and unable to switch to adequate therapy and therefore went into HHS.
Principles of Tx: IV fluids, Insulin, and Potassium. Both DKA and HHS are not conditions that have preset fluids or dosing of insulin or potassium. Labs must be monitored frequently and treatment titrated accordingly. (DKA and HHS algorithm links below). Another important note is that the fluid management is done differently in pediatrics than adults.
The reason I picked this case is because DKA and HHS are both prevalent complications with substantial morbidity and mortality; In the era of everybody having diabetes, it's good to be able to recognize and treat these conditions. These are also medical emergencies. It is not the hyperglycemia that causes the damage and death, but more often it is the inciting infection or complications such as cerebral edema that cause the most harm. Don't just assume the cause is poor insulin management, be sure to rule out common causes like pneumonia and UTI.
I hope this was helpful. If you have suggestions on things you'd like to see or do differently. Let someone from our class know. Thanks.
HHS Algorithm: http://www.uptodate.com.ezproxy.uthsc.edu/contents/image?imageKey=ENDO/67368&topicKey=ENDO%2F1795&source=outline_link&search=dka+hhs&utdPopup=true
DKA Algorithm: http://www.uptodate.com.ezproxy.uthsc.edu/contents/image?imageKey=ENDO/61747&topicKey=ENDO%2F1795&source=outline_link&search=dka+hhs&utdPopup=true