32 Y/M with Generalized Tonic Clonic Seizures and hypoglycemia
This case has been given to solve in an attempt to understand and analyse the patient's clinical data, and develop my competency in reading and comprehensive study on the clinical data including history, clinical findings, investigations, and coming up with diagnosis and treatment plans. This is an online e-log book to discuss our patient's de-identified health data shared after taking his / her / guardians' signed informed consent. Here we discuss our individual patients' problems through a series of inputs from the available global online community of experts with an aim to solve those patients' clinical problems with collective current best evidence-based information.
MED CASE:
32 year old male with generalized tonic clonic seizures and hypoglycemia.
CHIEF COMPLAINTS:
The patient was brought to casualty with loss of speech, generalized tonic clonic seizures and hypoglycemia 2 days ago.
HISTORY OF PRESENTING ILLNESS:
Patient was apparently alright 10 days back and then he got loose stools 7-8 episodes per day, yellowish in color, mucoid, foul smelling, non blood tinged
C/o pain abdomen in the epigastrium twisting type, aggravated on taking food
the patient had stiffening of bilateral UL and LL associated with up rolling of eyes in an unresponsive state, 2 episodes of involuntary micturition present, no tongue bite and drooling of saliva, his GRBS was low (33 mg/dl) and after dextrose infusion the patient became responsive.
No C/O chest pain, palpitations, SOB, vomitings.
PAST HISTORY:
K/C/O DM 2 since 1 year on GLIMI m1 PO BD 10 days inj mixtard 20 U——-10U . He stopped talking the medications 15 days prior to admission.
Patient was diagnosed to have pulmonary TB by a local hospital and was advised to take anti -TB medications (HRE) since 2 months.
He is diagnosed with acute pancreatitis almost 1 year ago which later progressed to chronic calcific pancreatitis (30 august,2023).
patient also has a h/o hsv infection since 3 months probably due to immunosuppression with regards to his above mentioned medical conditions.
Not a known case of CVA, CAD, thyroid disorders, Asthma, Epilepsy.
FAMILY HISTORY:
Father is a known case of TB 4 years ago
PERSONAL HISTORY:
Patient consumes alcohol 3-4 quarters per day, since 10 years.
Poor nutrition following the drinking.
Patient takes mixed diet. He has java for breakfast, and rice and curries for lunch and jonna roti for dinner, which consists of poor nutrition.
Appetite is adequate.
He also consumes khaini once a day since 1 year.
Sleep is inadequate when he doesn't consume alcohol.
Bowel and bladder activity is normal.
GENERAL EXAMINATION
The patient was conscious, coherent, cooperative,
Well oriented
He is malnourished and poorly built
Pallor present
Clubbing present- stage 3
Lymphadenopathy present: posterior cervical node palpable
No cyanosis, edema
BP = 100/70 MMHG
PR= 76 BPM
RR = 20 CPM
SPO2 = 98%
GRBS = 198 mg/dl
SYSTEMIC EXAMINATION:
CVS: s1, s2 heard, no murmurs
RS: bae +, reduced breath sounds on right side
Signs of volume loss present on the right side
P/A: soft, tenderness present in epigastrium
Skin: Keloid present on the chest, post inflammatory hyper pigmented macules (Herpes infection ) 3 months ago.
CNS examination
Tone: UL rt- N lt-N
LL rt- N lt-N
Power: UL rt- 5/5 lt- 5/5
LL rt- 5/5 lt- 5/5
Reflexes:
Biceps rt +2 lt +2
Triceps rt +2 lt +2
Supinator rt +1 lt +1
Knee rt+2 lt +2
Ankle rt +1 lt +1
Autonomic nervous system examination:
Isometric exercise - for increase in diastolic bp- no significant increase seen
Supine bp- 106/66
Standing bp(after 3 mins if standing without any support)- 110/70
Orthostatic hypotension - not seen.
INVESTIGATIONS:
18/09/2023
CUE:
COLOUR Pale yellow
APPEARANCE Clear
REACTION Acidic
SP.GRAVITY 1.010
ALBUMIN +
SUGAR Nil
BILE SALTS Nil
BILE PIGMENTS Nil
PUS CELLS 2-4
EPITHELIAL CELLS 2-3
RED BLOOD Nil
HEMOGRAM:
HAEMOGLOBIN #10.1
TOTAL COUNT # 14,500
NEUTROPHILS #82
LYMPHOCYTES #11
EOSINOPHILS 01
MONOCYTES 06
BASOPHILS 00
PCV #30.2
MC V #75.5
MCH #25.3
MCHC 33.4
RDW-CV 12.0
RDW-SD 33.6
RBC COUNT #4.0
PLATELET COUNT 2.72
LFT:
Total Bilurubin 0.68
Direct Bilurubin 0.15
SGOT(AST) #85
SGPT(ALT) 36
ALKALINE PHOSPHATE # 447
TOTAL PROTEINS #5.7
ALBUMIN #3.31
A/G RATIO 1.38
RFT:
SERUM CREATININE: 0.9
Blood Urea 11
CALCIUM 9.1
SODIUM 134
POTASSIUM 2.2
CHLORIDE 101
CALCIUM IONIZED 1.07
RBS #78
Test Result
BLOOD GROUP : O
RH TYPING : POSITIVE (+VE)
SERUM AMYLASE 47
SERUM LIPASE 18.0
SPOT URINE PROTEIN 10.9
SPOT URINE CREATININE 23.7
RATIO 0.45
Prothrombin Time 15 Sec
INR 1.11
ESR 16
BLEEDING TIME 2 Min 30 sec
CLOTING TIME 4 Min 30 sec
APTT TEST 31 Sec
ABG:
PH 7.43
PCO2 27.7
PO2 107
HCO3 18.1
St.HCO3 20.7
BEB -4.5
BEecf -5.4
TCO2 35.9
02 Sat 97.2
02 Count 18.0
--------------------------------------------------------------------------
19/9/2023:
SERUM MAGNESIUM 2.1
HEMOGRAM:
HAEMOGLOBIN #9.0
TOTAL COUNT # 12,000
NEUTROPHILS #89
LYMPHOCYTES #09
EOSINOPHILS 01
MONOCYTES #01
BASOPHILS 00
PCV #27.1
MCV #76.3
MCH # 25.4
MCHC 33.2
RDW-CV 12.1
RDW-SD 34.1
RBC COUNT #3.55
PLATELET COUNT 1.86
RFT: (Electrolytes)
SODIUM 137
POTASSIUM ##2.7
CHLORIDE 102
CALCIUM IONIZED 1.14
RFT:
Serum Creatinine 0.9
Blood Urea 12
SODIUM 141
POTASSIUM 3.0
CHLORIDE 102
CALCIUM IONIZED 1.18
ECG:
USG ABDOMEN :
IMPRESSION:
- Altered echotexture of pancreas and hyperechoic foci.
- Correlate with serum amylase and lipase levels
- Grade 2 fatty liver
- Right Renal cortical cyst.
2D ECHO :
IMPRESSION:
- No RWMA.
-Trivial TR and AR +. No MR
- No AS/MS.
- EF =60. RVSP = 32 MMHG
- Good LV systolic function
- No Diastolic dysfunction
- No PAH/ PE
- IVC SIZE (1.41 cms) collapsing.
DIAGNOSIS:
1. Adrenal insufficiency secondary to:
a) pulmonary TB
b) HSV infection (post infection)
2. Generalized tonic seizures secondary to hypoglycemia
3. Hypokalemia
4. Pulmonary TB since 3 months (on HRE)
5. Chronic calcific pancreatitis
6. K/c/o Diabetes mellitus type 2 since 1 year
TREATMENT:
1. IV fluids - NS, RL, DNS @ 100ml/hr
2. Iv pan 40 mg IV/OD
3. Inj KCL 2 amp(40mcg) in 500 ml NS over 5 hours
4. Inj calcium gluconate 1g in 100 ml ns IV
5. Inj MgSO4 2g in 100ml NS slow IV
6. HAI through S/C.
7. Tab isoniazid -225 mg
Rifampicin- 450mg
Ethambutol-825mg
8. Syp. potchlor 15 ml in one glass of water
Blooms learning levels:
1. Remembering:-
The basic history and sequence of events of the patient are remembered
patient was hypoglycemic and hypotensive and therefore , immediately started on D25 IV in casualty. This improved the patient's condition and he was responsive.
Patient had very low grbs as well (70 mg/dl) which was not improving completely despite D25 infusion. Later he was given hydrocortisone which slowly improved his glucose levels.
After a series of IV fluids and treatment mentioned above, the blood pressure has improved to 100/70 mmHg and GRBS to 198 mg/DL.
2. Understanding:-
Understanding the current problem of the patient and explained the ideas and concepts regarding the patient .
Most cases were in the category of 0–2mM glucose. The majority of cases had coma, a generalized tonic–clonic seizure was only observed when the s-glucose dropped below 2.0mM (1.2 mM). Two cases with focal seizure were noted: one patient had an s-glucose level of 2.0 mM, and the other patient 3.3 mM.
The mean age of patients with neuroglycemic symptoms was 54 years (range 20–87 years), and the mean age of patients without neuroglycemic symptoms was 64 years (range 2–95 years).
Twelve out of fourteen patients with neurological symptoms had diabetes mellitus and were treated with insulin alone or in combination with oral antidiabetic drugs.
Co-morbidity with alcoholism, or severe illness were contributing factors in the patients with seizures.
3. Applying
Based on the history of proper investigations,
ABG, RFT, LFT, RBS, ECG ; CXR ; ultrasound can be done.
AND everything is applied to give proper treatment to the patient.
Patients with adrenal insufficiency often present with hypotension, altered mental status, anorexia, vomiting, weight loss, fatigue, and recurrent abdominal pain.
The diagnosis of primary adrenal insufficiency requires suspicion as it mostly presents with non-specific symptoms. Hyponatremia and hypoglycemia may be present. Serum cortisol, ACTH, renin, aldosterone, and chemistry panel should be obtained. Serum cortisol level can help make diagnoses in the presence of elevated ACTH and plasma renin activity. The ACTH stimulation test can be performed to determine if the cause is central or peripheral.
3. Analyzing
Based on all the above levels she has Been analyzed properly to get a proper diagnosis for which adequate treatment is being given.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5712398/
After corticosteroid injection, patients with well-controlled diabetes experience smaller elevations and faster return to baseline glucose levels than patients with poor control. Insulin dependent diabetics experienced similar findings as patients with poor control. Future studies are needed to evaluate dosing to optimize the risks of blood glucose elevation while maintaining therapeutic benefit.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7051808/
Hypoglycemic attack is a clinical syndrome whereby a low glucose level results in neurogenic (adrenergic and cholinergic) or neuroglycopenic signs. Although a diverse etiology can lead to hypoglycemia, hypoglycemic agents are the main cause.
Although hypoglycemia can be quickly restored by carbohydrate supplementation in most cases, determining the underlying etiology is a crucial issue especially in patients without diabetes mellitus.
This is because adrenal insufficiency, a possibly life-threatening condition, can be latent.
Adrenal insufficiency is latent in patients with hypoglycemia episodes. Because patients with adrenal insufficiency require appropriate perioperative corticosteroid supplementation, clinicians should give priority to identifying the underlying etiology of hypoglycemia over non-urgent elective surgery when these co-occur.
LEARNING POINTS:-
1. Correlation of hypoglycaemia and hypotension with adrenal insufficiency
2. Affects of alcohol abuse on pancreas and the metabolic derangements that follow.
https://www.mdpi.com/2077-0383/9/6/1901
Chronic alcohol consumption alters essential micro- and macronutrient levels leading to a significant number of metabolic disorders, among which alcohol-related liver disease and pancreatitis are of the highest prevalence. The severity of alcoholic liver disease varies from simple steatosis to liver cancer. Patients with alcoholic liver disease should be encouraged to discontinue alcohol consumption. Alcohol administration is associated with increased damage due to oxidative stress and significantly lowered trace elements and antioxidant enzyme levels. There is a multitude of causes of the abovementioned imbalances, including inappropriate nutritional status, alcohol-related gastrointestinal disorders, diarrhea, vomiting, or excessive urination. Electrolyte and trace element imbalances are observed both during alcohol administration and alcohol withdrawal because of the defective functioning of renal tubules impaired by alcohol. The most common distortions include hypophosphatemia, hypomagnesemia, hypokalemia, hypocalcemia, and hyponatremia, as well as decreased levels of selenium, chromium, and zinc.
QUERIES DURING OSCE:
Q: What is causing hypoglycemia in the patient?
A: Patient is a known case of diabetic with a history of non-compliance to diabetic medications. Also, he is a chronic alcoholic since 10 years which contributes to hypoglycemia. He is also malnourished with a history of poor nutrition which could also contribute to his condition.
Q: How do we treat this problem?
A: The patient should be given insulin and dextrose infusion to help him recover from Hypoglycemia and also prevent hyperglycaemia. While giving corticosteroids treatment, it is crucial to monitor his vitals. Timely blood glucose and blood pressure monitoring should be done to keep them under control.
Since he has chronic pancreatitis, it is important to check his electrolyte imbalances and provide the deficits through treatment.
However, it is important to stabilise the patient and slowly correct his imbalances and nutrition deficits. Patient education should be encouraged to help him abstain from alcohol consumption by psychiatric counselling and management. His nutritional intake also should be changed to prevent further malnourishment which could make him susceptible to various infections and other diseases.
Q: what is the cause of hypotension in the patient?
A:
Patients with adrenal insufficiency often present with hypotension, altered mental status, anorexia, vomiting, weight loss, fatigue, and recurrent abdominal pain.
The diagnosis of primary adrenal insufficiency requires suspicion as it mostly presents with non-specific symptoms. Hyponatremia and hypoglycemia may be present.
This explains why the patients glucose levels have improved and hypotension has resolved, when the patient was given hydrocortisone treatment.
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