I've been given this case to solve in an attempt to understand the topic of "patient clinical data analysis" to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and come up with a diagnosis and treatment plan.
You can find the entire real patient clinical problem in this link here..
https://hitesh116.blogspot.com/2020/05/elog-13th-may-2020.html?m=1
Following is my analysis of this patient's problem:
Current issues or chief complaints of the patient.
The problems in order of priority I found are
1) difficulty in walking since 1 month
2) bilateral lower limb weakness since 1month
3)pain in lower limb calf muscles since 1 month
4)fever since 1 week
NOTE: As the patient presented with acute onset paraparesis we need to rule out all of the causes.
So the differential diagnosis for acute onset paraparesis :
1. Extramedullary lesions :-
a) spinal trauma
b) pathological fractures
c) epidural abscess
d) Dural AVM
2. Intramedullary lesions:-
a)demylinating :- multiple sclerosis,
acute disemminated encephalomyelitis
b) ischemia:- infarction - trauma , thromboembolism
Haemorrhage- vasculitis
c) myelitis :- viral, bacterial , parasitic(schistosomiasis).
Reference: www.kznhealth.gov.za/medicine/presentation 48.pdf
Investigations to be done: blood investigations , structural investigation, csf examination
1-ANATOMICAL LOCATION OF THE PROBLEM:!
We observed that there is hypotonia,hyporeflexia,flaccid paralysis are seen a characteristic of LMN LESION(LOWER MOTOR NEURON)
Deep tendon reflexes
Right. Left
Biceps. P. ---
Triceps. ---. ---
Supinator. --- ---
Knee --- ---
Ankle. --- ---
Tone: ul. normal. Normal
LL. hypotonia. hypotonia
Power :almost all the muscles in the leg are showing 3/5 power indicating flaccid paralysis.
SPECIFIC ANATOMIC LOCATION:
Specific anatomical location should be studied to know whether the disease is from either 1)neurogenic 2)myogenic or 3) neuromuscular junction
1)if suspecting myogenic cause then creatine kinase and muscle biopsy should be done.
CREATININE KINASE- 92 IU/L which is normal so muscle related cause is ruled out.
2)If suspecting Neuromuscular junction cause then electromyography should be done which is also normal in this case so it is ruled out.
3)if suspecting neurogenic cause then..
Nerve conduction studies should be done.
The study shows
Bilateral common peroneal and sural nerve axonal neuropathy(peripheral neuropathy)Investigations:
NERVE CONDUCTION STUDIES:
2-PHYSIOLOGICAL FUNCTIONAL DISABILTY
as there is axonal degeneration of neurons there will be functional disability of these nerves resulting in
-progressive weakness or clumsiness
-difficulty in walking
-absence of reflexes or diminished
3-ETIOPATHOLOGY
FROM the history of the patient he is alcoholic and there is anaemia. Due to alcohol consumption there is deficiency of vitamins like b1,b3,b6 which is one of the cause of peripheral neuropathy.
Calf pain is most common in ALCOHOLIC NEUROPATHY. Due to this there will be metabolic disturbances where there is accumulation of fructose and sorbitol in Schwann cell causing axonal degradation.
https://www.slideshare.net/mobile/meducationdotnet/peripheral-neuropathy-57320857link
Other viral etiology are ruled out using investigation.
4-Other problems faced
Pain and fever
The cause of pain may be due to inflammation of these nerves and fever may be due to any infection which is not ruled out. Csf examination is necessary to rule out the causes of myelitis and other possible causes.
5.TREATMENT PLAN
a)pharmacological component
1-T pcm 650 mg thrice daily for fever
2-inj neomol 100ml IV infusion if fever greater than 101° f
3-T.bcomplex once daily for peripheral neuropathy
4-permethrin 5% lotion for scabies
b) non pharmacological component
Physiotherapy and proper diet should be made..!!
References: Dr. Hiteesh s presentation and blog .
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