Signalment:
9 year old spayed female golden
retriever
Presenting complaint:
Found collapsed outside, now having
seizures
Presenting History:
The patient was previously diagnosed
with diabetes mellitus 3 months prior to presentation. She had
been eating normally and had a recent change in her insulin
regimen. Her insulin dose was increased from 22 units to 24
units of NPH based on results of blood glucose curves and
clinical response. She was pu/pd at 22 units, and drinking and
urinating normally 24 units. She had what was described as a
hypoglycemic event approximately one month prior to
presentation, however when she was tested at that time by her
regular veterinarian, her blood glucose was low normal according
to her owner. Yesterday, approximately 2 hours after she
received her evening dose of insulin, she was panting and was a
mildly weak. Her owner gave her some additional food (which she
ate well) and the weakness resolved. This morning, she was
acting normally and ate well. Her owner gave her the morning
dose of insulin. She was observed to be normal during the
afternoon, however when the owners came home from work they
found her unconscious and non-responsive under a bush. There
was no known history of trauma or dietary indiscretion, however
she is housed outside and was not supervised for a several hours
prior to presentation. She is up to date on her vaccinations
and has no other previous pertinent medical history.
Physical exam findings:
Subjective:
Comatose, 3-5% dehydrated. Body
condition score: 3/5
Objective:
EENT: pupils miotic but equal and
responsive to light. There was some brown material on her
tongue (didn’t smell like vomit – r/o dirt).
Heart/lungs: NSF
Lymph nodes: NSF
Skin: NSF
Abdomen/urogenital: NSF
Rectal exam: fine pieces of
grass/mulch in her feces
Musculoskeletal: laterally recumbent,
otherwise unremarkable.
CNS: comatose, no seizures on
presentation. Unable to assess cranial nerves or peripheral
nervous system besides reflexes, which were within normal limits
Assessment:
13 year old spayed female golden
retriever with historical diabetes mellitus.
Comatose with mild dehydration on
presentation
Rule outs:
Hypoglycemic coma
Toxin ingestion
Trauma
Neoplasia (primary CNS vs
extra-cranial)
Hypertension
Hypotension
Cardiac arrhythmia
Hypoadrenocorticism
Thromboembolic disease
Infectious (viral, bacterial,
parasitic, or fungal) disease
Plan (initial):
Provide flow by oxygen and maintain a
patent airway (patient was breathing on her own). Obtain
samples to assess blood glucose.
Obtain a complete blood count,
biochemical profile, blood gas, and urinalysis.
Hold samples for urine culture, tick
titers, toxoplasmosis titers, etc. Monitor blood pressure and
cardiac rhythm (continuous ECG). Place intravenous (IV)
catheter, initiate IV fluids (and supplemental dextrose as
necessary). Monitor level of consciousness. Obtain thoracic
and abdominal survey radiographs. Provide supportive care
(lubricate eyes and turn frequently while unconscious).
Laboratory diagnostic results and
resulting treatments:
Time |
Blood gluc-ose |
Mental Status |
ECG |
Treatment |
0 (10:00pm) |
25 |
Comatose |
Intermittent VPCs with sinus tachycardia |
One liter crystalloid bolus, followed by 50 ml 25%
dextrose bolus and 15mg diazepam administered
intravenously initially; flow by oxygen was administered
and a continuous infusion of LRS + 2.5% dextrose at 1.5
times maintenance was started. |
0.5hr (10:30pm) |
|
Comatose, seizure and tremor activity noted |
Ventricular tachycardia |
Diazepam 15mg IV for initial grand mal seizure activity
and then severe facial twitching ( two additional doses
were given 5 and 10 minutes after this first dose);
Dextrose infusion was increased from 2.5% to 5% |
1.5hr (11:30pm) |
18 |
Comatose, seizure and tremor activity noted |
Ventricular tachycardia |
Propofol 100mg IV slow bolus given to stop
seizure/tremor activity (good response to treatment -
resolution of signs); increased dextrose infusion to
7.5% from 5%, an additional 40ml dextrose in 120ml 0.9%
NaCl (due to low blood glucose) and 15mg diazepam (due
to breakthrough paddling/seizure activity) were given |
2hr (12:30am) |
29 |
|
|
|
2.5 hr (1am) |
37 |
Comatose |
Ventricular tachycardia |
An additional bolus of 40ml 50% dextrose diluted with
120ml O.9% NaCl was given |
2.6hr (1:10am) |
264 |
|
|
|
3.1hr (1:40am) |
71 |
|
|
|
3.5hr (2am) |
45 |
|
|
Increased dextrose infusion from 7.5% to 10%; 10mg
dexamethasone sodium phosphate and an additional 40ml
50% dextrose diluted with 80ml 0.9% NaCl were
administered |
4.5hr (3am) |
161 |
Comatose; seizure activity noted |
Ventricular tachycardia |
Repeat grand mal seizure occurred and since blood
glucose was normal at this point, a propofol CRI was
started (0.1mg/kg/minute to start) to treat this; a
lidocaine bolus (2mg/kg) was given to try to covert to
normal sinus rhythm |
5.5hr (4am) |
98 |
Comatose |
Ventricular bigeminy with intermittent runs of ventricular
tachycardia |
Lidocaine CRI was started at 0.05mg/kg/minute with an
initial additional bolus of 2mg/kg lidocaine to
reconvert |
7.5hr (6am) |
158 |
|
Ventricular bigeminy |
|
9.5hr (8am) |
50 |
Comatose to stuporous |
Rare VPCs |
Arterial blood gas showed elevated PCO2; propofol CRI
weaning was started in an attempt to improve ventilation
ability |
10.5 hr (9am) |
77 |
Comatose to stuporous |
Intermittent VPCs with sinus tachycardia |
|
11.5 hr (10am) |
65 |
Stuporous |
Rare VPCs |
Improved PCO2 on arterial blood gas with propofol CRI
tapering, no breakthrough seizure activity |
15hr (1:30pm) |
58 |
Depressed to stuporous |
Rare VPCs |
Continued to decrease propofol CRI (no seizure activity) |
17.5hr (4pm) |
102 |
|
Rare VPCs |
|
19.5hr (6pm) |
|
Depressed to stuporous |
Rare VPCs |
Discontinued propofol CRI |
21hr (8pm) |
93 |
Depressed to stuporous |
normal sinus rhythm |
On 10% dextrose CRI with LRS, lidocaine CRI (at
0.05mg/kg/min) (as started at 2am and 4am respectively),
on nasal oxygen |
25hr (11pm) |
44 |
Brief seizure/tremor activity |
normal sinus rhythm |
|
26hr (12am) |
74 |
Brief seizure/tremor activity |
normal sinus rhythm |
IV bolus of 60mg propofol was administered and she was
then restarted on propofol CRI at 0.07mg/kg/minute |
31hr (5am) |
94 |
Brief seizure/tremor activity |
normal sinus rhythm |
IV bolus of 60mg propofol was administered for
breakthrough seizure activity |
36hr (10am) |
155 |
Depressed to stuporous |
normal sinus rhythm |
Discontinued lidocaine CRI (still on nasal oxygen,
propofol 0.07mg/kg/minute and LRS +10% dextrose at
maintenance rate) |
Overall diagnostic lab work findings
as drawn on presentation:
Complete Blood Count
WBC: 15.47 m/mm3 (6.0 - 17.0)
LYM: 0.70 # (1.0 - 4.8)
MON: 0.98 # (2.0 - 10.0)
GRA: 13.78 # (3.0 - 12.0)
LYM%: 4.6 % (12.0 - 30.0)
MON%: 6.4 % (0.1 - 7.0)
GRA%: 89.1 % (62.0 - 87.0)
RBC: 6.86 M/mm3 (5.5 - 8.5)
HGB: 16.6 g/dl (12.0 - 18.0)
HCT: 45.67 % (37.0 - 55.0)
MCV: 67 fl (60.0 - 77.0)
MCH: 24.3 pg (19.5 - 24.5)
MCHC: 36.4 g/dl (31.0 - 34.0)
RDWc: 15.8 (8.0 - 12.0)
PLT: 440 m/mm3 (200 - 500)
PCT: 0.37 %
MPV: 8.5 fl (5.0 - 12.0)
PDWc: 38.4
Diagnostic Profile - *blood drawn
prior to any dextrose administration*
ALB: 3.6 (2.5 - 4.4) G/DL
ALP: 88 (20 - 150) U/L
ALT: 109 (10 - 118) U/L
AMY: 550 (200 - 1200) U/L
TBIL: 0.2 (0.1 - 0.6) MG/DL
BUN: 24 (7 - 25) MG/DL
CA++: 10.3 (8.6 - 11.8) MG/DL
PHOS: *1.3 (2.9 - 6.6) MG/DL
CRE: 0.6 (0.3 - 1.4) MG/DL
GLU: *25 (60 - 110) MG/DL
Na+: 151 (138 - 160) MMOL/L
K+: 4.2 (3.7 - 5.8) MMOL/L
TP: 6.9 (5.4 - 8.2) G/DL
GLOB: 3.3 (2.3 - 5.2) G/DL
HEM: 2+, LIP: 1+, ICT: 0
Blood Gas / Electrolyte (IRMA)
Patient Temperature: 102.2
BP: 758 mmHg systolic
Measured @ 37.0 degrees C
pH 7.461
pCO2 28.4 mmHg
pO2 95.0 mmHg
Temperature corrected to values
pH 7.430
pCO2 31.0mmHg
pO2 107.4 mmHg
Measured
Hct 48.6 %
Na+ 149.4 mM
K+ 3.45 mM
iCa 1.13 mM
Calculated results
HCO3- 20.0 mM
TCO2 20.8 mM
BEb -2.4 mM
BEecf -3.8 mM
O2Sat 97.5%
tHb 16.5 g/dL
tHb for BEb 15.0 g/dL
Urinalysis - Method of Collection:
urinated and was caught into sterile container
Color: yellow
Turbidity: clear
Specific Gravity: 1.015
Urobilinogen: neg
Glucose: negf
Ketones: neg
Bilirubin: neg
Protein: +300
Nitrite: Neg.
Leukocytes: neg
Blood: LARGE
pH: 7.5
Sediment:
RBC: 30-50 per hpf
WBC: neg per hpf
Bacteria: none seenFat: eg per hpf
Sperm: neg per hpf
Debris: neg per hpf
Casts: none seen
Cells:
Squam. Epith.: g per hpf
Trans. Epith.: nnn per hpf
Renal: n per hpf
Crystals: none seen
Imaging results:
No radiographs were obtained
during her hospitalization.
ULTRASOUND REPORT
Primary Concern: Diabetes mellitus
hypoglycemic coma - now stuporous
recurrent refractory hypoglycemia
hypercapnia
mild hypertension (340mmHg initial
reading this AM was spurious)
recurrent seizures (even after blood
glucose had been stabilized)
cardiac arrhythmias (now only
infrequent VPC's - had been much worse overnight), now has
intermittent bundle branch
block
Date of Ultrasound: Wednesday,
September 21, 2005
Area Scanned: Abdomen
Specific Findings:
Liver: The
liver is diffusely mildly hyperechoic, rounded and slightly
irregular in contour with a few small~1cm hypoechoic nodules.
Gallbladder / Biliary Tract: WNL
Spleen: WNL
Kidneys: ~7cm with a faint hypoechoic
subcapsular rim and mildly hyperechoic cortices.
Urinary Bladder: Trace echogenic
debris.
Prostate: N/A
GI Tract: The stomach contains a
small amount of fluid. The SI are WNL.
Pancreas: The pancreas is visible,
mildly hyperechoic with a small ~0.6cm irregular hyperechoic
focus and a small ~0.44cm hypoechoic nodule.
Lymph Nodes: None seen.
Reproductive Organs: N/A
Adrenals: 0.6cm WNL.
Diagnostic Impressions: Liver
findings are nonspecific R/O changes secondary to DM, steroid
hepatopathy or nodular hyperplasia. Biopsy need for a definitive
diagnosis. Pancreatic findings are most consistent with previous
pancreatitis and nodular hyperplasia. Can not R/O an insuloma
but there was no mass visible to support this DDX. Renal changes
R/O interstitial nephritis. The hypoechoic outer rim may be the
result of fluid therapy.
Ultrasonographer:
Leslie Schwarz, DVM
Diplomate, American College of
Veterinary Radiology
Treatment and clinical progression:
For specific treatment, see chart
above. Additional supportive care including flow by and nasal
oxygen, indwelling urinary collection system, soft bedding,
passive range of motion and turning frequently (to reduce the
chance of decubital ulcers) and ocular lubrication were also
provided.
Outcome: Molly was transferred to a
neurology service where she had an MRI which was unremarkable.
She continued to make slow progress towards recovery and was
eventually discharged to her owners’ care when she was
ambulatory but still non-visual. She did continue to have
infrequent seizures. She was discharged on a lower dose of
insulin and Phenobarbital.
Final diagnosis: Severe hypoglycemic
event with lasting neurologic consequences likely secondary to
cerebral edema from neuroglycopenia.
Discussion:
Hypoglycemia, whether from insulin
overdose (endogenous or exogenous), increased consumption (neoplasia,
sepsis or severe polycythemia) or from insufficient production
(as seen in pediatric patients, in some sporting breeds, or in
patients with liver disease, hypoadrenocorticism, glycogen
storage diseases, starvation or portosystemic shunts/liver
disease) can cause neurologic consequences such as was seen in
this case. Progressive or persistently low serum glucose
causes central nervous system vasoconstriction and decreased
oxygen delivery in addition to decreased glucose delivery. This
causes neuronal dysfunction and eventually neuronal death. The
patient may be left with transient or persistent cortical
blindness or seizures post-episode.
Patients presenting with a primary
complaint of weakness, tremors, disorientation, behavior
changes, seizures or coma should have their blood glucose
checked on presentation. If the glucose is found to be below
60mg/dl, patients should be offered high protein food (such as
Hill’s a/d or Eukanuba Max-Calorie) if they are conscious. An
IV catheter should be placed, and 2-4ml/kg of 25% dextrose
should be administered intravenously as a bolus. Their blood
glucose should be monitored regularly (every hour or more
frequently in the emergent period) and the patient should be
started on a CRI of dextrose (can be given as part of their
fluid requirements as was seen here) to a maximum of 20%.
Higher than 25% dextrose given intravenously can cause severe
phlebitis therefore should be avoided. If an insulin secreting
tumor is suspected, small doses of dextrose given as needed
(monitoring the blood glucose with serial testing) should be
attempted as large doses may stimulate the tumor causing larger
releases of insulin, initiating a vicious cycle. If the patient
does not regain consciousness and/or continues to seizure, this
may be suggestive of cerebral edema secondary to neuroglycopenia.
Additional treatment with mannitol may be necessary if this
occurs to reduce further brain swelling. Once a patient has
been stabilized, further diagnostics should be done in an effort
to determine the etiology of the hypoglycemia.
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