Case based OSCE along with Bloom's learning levels acheived
OSCE DAY:
I was asked to take up two cases for the OSCE.
One case from OP and one from IP, i. e., ICU.
The OP case was about a 30 year old female with complaint of headache, and the IP case was about a 32 year old male with Generalized Tonic Clonic Seizures in ICU.
First, I was assigned an OP case to do history taking and physical examination of the patient. I further diagnosed and assisted the patient in recieving the treatment for her complaint as well.
Here is the case as presented below.
CHIEF COMPLAINT :
30 year old female patient walked in to OP room with complaint of frontal headache since 4 days.
HISTORY OF PRESENT ILLNESS:
30 year old female patient walked in to OP room with complaint of frontal headache since 4 days.
She has a history of trauma 4 days back since then she developed the headache. Her symptom was associated with photophobia and photophobia.
She has no complaints of loss of consciousness, giddiness, blurring of vision, fever, nausea and vomitings.
No complaints of cold, cough, chest pain, SOB, burning micturition, loose stools, pain abdomen.
PAST HISTORY:
She is a known case of Hypothyroidism and on tab thyronorm 50 mcg since 2 years
She is not a known case of HTN, Asthma, TB, epilepsy, CVA, CAD.
She has a history of head trauma 6 months back. The same incident happened 6 months back where she had History of head trauma which was followed by front headache which didn't subside upon taking medication prescribed by local hospital.
GENERAL EXAMINATION:
PT IS CONSCIOUS, COHERENT AND COOPERATIVE
Mild PALLOR present
No ICTERUS
No CLUBBING
No CYANOSIS
No LYMPHADENOPATHY
No EDEMA
TEMP- AFEBRILE
BP- 100/60 MM HG
PR- 76 BPM
RR- 18CPM
SYSTEMIC EXAMINATION:
CVS - S1 S2 HEARD. NO MURMURS
RS- BLAE +, NORMAL VESICULAR BREATH SOUNDS. NO ADDED SOUNDS HEARD.
ABDOMEN EXAMINATION:
Inspection:
Abdomen is soft and flat.
No sinuses,scars, pulsations, peristalsis.
Umbilicus is central and inverted.
All quadrants of Abdomen move equally with respiration.
Palpation:
Abdomen is soft on palpation and no tenderness noted in any quadrants.
Percussion:
Resonant note is heard on percussion
shifting dullness negative
Auscultation:
Bowel sounds are heard.
CNS- NO FOCAL NEUROLOGICAL DEFICITS.
Diagnosis: Frontal headache
COURSE IN THE HOSPITAL:
Patient was advised to get an ophthalmology check up for the headache. I took her to ophthalmology OPD and get her eye examination done. They have revealed that she has mild refractive error (-0.25 in right and left eye) which can be corrected by spectacles. Hence, she was provided a pair of eyeglasses and advised to use it daily. This would eventually subside her headache as well.
TREATMENT:
1. TAB PARACETAMOL 650 MG PO/SOS
2. SPECTACLES WITH POWER OF -0.25 FOR BOTH EYES , FOR DAILY USE.
LEARNING POINTS:
https://pubmed.ncbi.nlm.nih.gov/16501409/
In a masked case-controlled study, we investigated the four aspects of refractive errors that have been implicated in the literature as correlated with migraine: spherical refractive error, astigmatic refractive error, anisometropia, and uncorrected ametropia. We also compared the calculated scalar value of refractive error, aided and unaided visual acuity, and spectacle use in migraine and control groups. We then investigated the relationship between refractive components and key migraine headache variables.
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After completing this, we proceeded to do OSCE on an IP case. We walked to ICU, where I was given opportunity to present the below case and learning interesting views about the case.
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 HAI 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
BP MONITORING
GRBS MONITORING
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
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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.
Indeed, patients with diabetes mellitus more frequently suffered from hypoglycemia than patients without diabetes.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. Herein, we present a case of secondary adrenal insufficiency where a single hypoglycemic attack just before elective surgery was the only complaint.
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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