Medical Cases

History: A 60 yr female with history of fall from 5 stairs at her residence. No history of LOC/ ENT bleed/ seizure/ vomiting/ FND. On examination B/L periorbital discoloration can be noted. What’s the likely diagnosis?

Answer: Raccoon eyes sign aka panda eyes is periorbital ecchymosis with sparing of the tarsal plate and is a physical examination finding indicative of a base of skull fracture of the anterior cranial fossa. It has positive predictive value of 85%. Also seen in metastatic neuroblastoma, Kaposi sarcoma, multiple myeloma, and amyloidosis.

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History: A 35 yr old male working with germicides accidentally came in contact with hydrofluoric acid presented to ED with blue-gray appearance with surrounding erythema of skin with extreme pain. How will you manage this in your ED?

Answer:  Decontaminate the patient by removing contaminated clothing and do copious irrigation for 15-30 mins.

• Apply 2.5 % Calcium gluconate gel LA.
• Inj 10% Calcium gluconate ID at rate of 0.5mL/cm2 OR 40 ml D5 + 10 mL 10%  calcium gluconate infusion over 4 hrs.

Clinical Rounds by ClinicHours

History: A 55 yr old male presented to ED with severe left-sided chest pain from 20 minutes radiating to the left arm associated with SOB and diaphoresis. Bp – 140/82mmhg, P – 84 bpm, spo2 – 92% on RA. ECG done. What’s the diagnosis?

Answer: Posterior MI is suggested by the following changes in V1-3:

• Horizontal ST depression
• Tall, broad R waves (>30ms)
• Upright T waves
• Dominant R wave (R/S ratio > 1) in V2

Posterior infarction is confirmed by the presence of ST elevation and Q waves in the posterior leads (V7-9). Leads V7-9 are placed on the posterior chest wall in the following positions (see diagram below):

Source: LITFL

OR you can invert the ECG to see a typical STEMI. For example:

Source: LITFL

The above patient was taken for thrombolysis after stabilization. ECG after thrombolysis.

Clinical Rounds by ClinicHours

History: A 67-year-old male k/c/o CKD-5 on MHD thrice weekly with Type2DM & HTN presented to ED with SOB, anasarca and AMS. P – 164 bpm irregular, SP02- 80 % on RA, RR – 30, R/E – B/L AE ↓ with B/L crepitations +nt. E3V2M5. ABG – pH 7.17, pCO2 9.7, Na+ 135, k+ 4.5, Lac 10.7, Glu 141, HCO3- 3.6. ECG was done. What’s the diagnosis?

Answer: ECG shows irregularly irregular narrow complex tachycardia with absent P waves & ST ↓ V4-V6 which is s/o Atrial fibrillation.

Classification is dependent on the presentation and duration of atrial fibrillation as below:

First episode – initial detection of AF regardless of symptoms or duration
Recurrent AF – More than 2 episodes of AF
Paroxysmal AF – Self-terminating episode < 7 days
Persistent AF – Not self-terminating, duration > 7 days
Long-standing persistent AF – > 1 year
Permanent AF – Duration > 1 yr in which rhythm control interventions are not pursued or are unsuccessful.

How will you manage the above patient in the ED? Write down in the comment section. 

Clinical Rounds by ClinicHours

History: A 47-year-old male was brought to ED in an unresponsive state with h/o 1 episode of seizure at home. He is k/c/o CKD5 on MHD twice weekly. BP – 200/120 mmHg, P -118 bpm, Sp02 – 92 % on RA. GCS – E2V1M4. B\L plantar – mute. RBS – 124 mg/dl. ABG (on o2 support) – PH 7.35 PCO2 34.4 PO2 106  HCO3 19.3 Lac – 4. NCCT head was done. What’s the diagnosis?

Answer: NCCT head reveals Intraparenchymal hemorrhage bleed with surrounding edema in left fronto-parieto-temporal, left gangliocapsular region and thalamus extending to the ventricular region with midline shift towards the contralateral side. The patient was intubated i/v/o low GCS and was admitted to the neurosurgery ICU after giving Inj. Levetiracetam 1.5 gm, Inj. Furosemide 40mg, IVF 3% Nacl.

Clinical Rounds by ClinicHours

History: A 8-month girl was brought to Dermatology OPD by her mother with a diffuse reddish macular lesion on the right side of her face present since birth. Lesion was smaller, lighter in colour & gradually increased in size. What’s the diagnosis?

Intro: Port wine stain (nevus flammeus) is a discoloration caused by a capillary malformation in the skin. Named after fortified red wine from Portugal.

Cause: Mutation in GNAQ gene on chromosome 9q21 & RASA1 gene. Associated with Sturge-Weber syndrome or Klippel–Trénaunay-Weber syndrome.

Types: Nevus flammeus nuchae, Midline nevus flammeus.

CF: Flat & pink asymptomatic macular patch usually seen at birth or may be acquired. Color may deepen to a dark red or purplish color in adults. Common sites are face, head, neck, abdomen, legs, or arms.

Dx: History based, skin biopsy, MRI Brain (R/O Sturge–Weber syndrome).

Rx:  Pulse Dye or Nd: YAG or KTP Laser, surgery excision, radiation, tattooing, rapamycin LA. If left untreated, these vascular lesions may deepen in color or may undergo hypertrophy & nodular thickening.

Clinical Rounds by ClinicHours

History: A 8 yr old boy came to the ED with accidental ingestion of an Endodontic file while having a dental procedure. Pt. was asymptomatic at the time of presentation with no SOB, abdominal complaints & vomiting. What’s the next step you will do in ED?

Answer: CXR -AP view & abdominal x-ray – Erect & supine was done on arrival after initial assessment. Pt. was hemodynamically stable. Pt was admitted to the surgery ward for observation. There were no signs of peritonitis or perforation. In this case, FB passed spontaneously with the stool on its own & no surgical intervention was required.

Foreign body ingestion is a common clinical problem. Commonly seen in children, older people, people with intellectual disability, psychiatric pathologies & prisoners/inmates.

Most ingested foreign bodies will pass through GI tract without symptoms & cause only minor mucosal injury. However, 10% – 20% of cases will require non-operative intervention, 1% may develop complications (e.g. bowel obstruction, perforation, severe hemorrhage, abscess formation, or septicemia) & require surgical interventions.

Look for dysphagia, abdominal pain, signs of peritonitis, stridor, wheezing, gagging, nausea/vomiting, neck/throat pain, atypical chest pain or non-cardiac chest pain, choking & LGIB.

Endoscopy is the first-line intervention for the removal of FB. However, Button battery ingestion can be potentially fatal and thus requires immediate intervention. Check out the management algorithm for sharp FB ingestion.

Clinical Rounds by Clinic Hours

History: A 56 yr old k/c/o CKD-5 on MHD thrice weekly with HTN presented to ED with SOB, drowsy, anasarca. He has missed his hemodialysis this week. BP-170/102 mmhg, P-84 bpm, Spo2 – 82% on RA (99% on NRBM 14/L O2), B\L crepts +nt. Serum K+ – 8.4 mmol/L. What’s the finding in ECG?

Answer: ECG shows sine wave appearance in severe hyperkalemia. Hyperkalaemia is defined as a serum potassium level of > 5.2 mmol/L. ECG changes generally do not manifest until there is a moderate degree of hyperkalaemia (≥ 6.0 mmol/L). The earliest manifestation of hyperkalaemia is an increase in T wave amplitude.

The patient was treated with 10% 10ml of IV calcium gluconate, nebulised with Salbutamol, 10 units of regular insulin IV combined with  dextrose 50%, IV sodium bicarbonate 50 mEq and Inj. Furosemide 40mg IV. Emergent haemodialysis was initiated. Pt was shifted to ICU.

Clinical Rounds by Clinic Hours

History: A 56 year old female presented to ED with 1 episode of GTC seizure. Neurological examination was normal except for postictal confusion. NCCT brain showed multiple calcified granuloma, some showing perilesional oedema in the frontal, parietal & occipital lobes. Routine CXR showed typical rice-grain-shaped calcification in the chest wall muscles. Xray thigh and forearm were ordered which showed similar lesions. What’s the diagnosis?

Clinical Rounds by ClinicHours

History: A 14 year-old boy presented with progressive proximal weakness of the lower limbs starting at 4 years of age followed by involvement of the upper limbs. He is the product of a consanguineous marriage. Clinically, he had flaccid quadriparesis with wasting and contractures without any sensory or neurological involvement. His weakness worsened leading to an inability to walk without support by the age of 8 and total wheelchair dependence by the age of 11. He was frequently admitted to hospital with chest infections. The patient’s creatine kinase was 2600 IU/L (normal 50–150 IU/L) and muscle biopsy from left quadriceps showed rounded small muscle fibres with evidence of degeneration and an absence of dystrophin protein. What’s the diagnosis?

Answer: Duchenne muscular dystrophy is a X-linked recessive genetic disorder.

Cause: Gene mutation of dystrophin protein.

Signs and symptoms: Muscle weakness, scoliosis, Respiratory Infections, Gowers’s sign.

Diagnosis: Creatine kinase (CPK-MM), DNA test, Muscle biopsy, Prenatal tests.

Treatment:

• Corticosteroids such as prednisolone and deflazacort lead to short-term improvements in muscle strength and function up to 2 years.
• The medication eteplirsen, a Morpholino antisense oligo for the treatment of mutations amenable to dystrophin exon 51 skipping.
• The medication ataluren (Translarna) is approved for use in the European Union.
• The antisense oligonucleotide golodirsen (Vyondys 53) was approved for medical use in the United States in 2019, for the treatment of cases that can benefit from skipping exon 53 of the dystrophin transcript.
• The Morpholino antisense oligonucleotide viltolarsen (Viltepso) was approved for medical use in the United States in August 2020, for the treatment of Duchenne muscular dystrophy (DMD) in people who have a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.
• Casimersen (Amondys 45) was approved for medical use in the United States in February 2021, and it is the first FDA-approved targeted treatment for people who have a confirmed mutation of the DMD gene that is amenable to exon 45 skipping.

Clinical Rounds by ClinicHours