A 23 year old male with lower limb weakness

I have been given this case to solve in an attempt to understand the topic of parient clinical data analysis to develop my competency in reading and comprehending clinical data including history,  investigation
 And come up with a diagnosis and treatment plan
Entire real patient clinical data is here:
https://vaish7.blogspot.com/2020/05/medicine.html?m=1

COMPLAINTS :
Bilateral lower limb weakness and sudden fall.
Vomiting
Gluteal, scrotal abscess(operated).

ANALYSIS:
Bilateral lower limb weakness since 5days associates with tingling , numbness.
There was history of sudden fall.

Causes may be
Trauma:ruled out no history  given
Vitamin deficiency-no features suggestive.

Sudden fall , numbness,tingling sensation may occur due stroke (tuberculosis)

Peripheral Neuropathy can be ruled out by nerve conduction studies.

Spondylodiscitis due infections (mainly TB )
Can be ruled out by mri ,  biopsy , pcr .

It may occur due to  tumors(meningiomas,gliomas,) ruled out by MRI, CT, ICP monitoring ,CSF analysis.

Spinal cord injury-sensory loss, bowel bladder incontinency,numbness and tingling. Which are ruled out by MRI,CT.

INVESTIGATIONS:  MRI OF BRAIN

 By this its shows there is significant enhancement representing meningeal enhancement or exudates and following regions with mri with multiple nodules in pulmonary apices  suggestive of pulmonary kochs, disseminated tuberculosis.

Vomitings occured 3days back ,
It may occur due to infections, drug intake toxins intake these all are ruled out because no history mentioned.
 Vomitings may be caused due increased intracranial tension caused due to tumors , infections.
 Gluteal abscess- which was operated 5months back.
Scrotal abscess-10 days back operated.


He has  history of multiple sexual parteners
Hiv testing-negative.

  Patient i found to have tuberculosis but didnt have classical findings.

FURTHER ANALYSIS: As the patient  found to have disseminated tb (mri) so  potts disease of spine should be evaluated.
It is important to rule out spondylodiscitis(main organism-mycobacterium tuberculosis).

ANATOMICAL SITE: lumbar vertebrae,(L4, L5), vertebral discs.

PHYSIOLOGICAL DISABILITY: bilateral lower limb weakness.

PATHALOGY: any infections spread to vertebrae through hematogenous or lymphatic spread cause damage to bones leading to compression  of nerves are damages leading to paralysis.(L4,L5 vertebrae) involvment.
As investigations suggusting disseminated  TB. So this infectionby hematogenous route  lead to involve ment of disc of vertebrae leading to destruction of surrounding structures (psoas abscess).
https://www.slideshare.net/mobile/wikadkaur/potts-disease-ppt
 TREATMENT:  anti tubercular treatment,   rest , physiotherapy.

A case of 18 yr old patient with bilateral limb weakness with edema

I have 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, inveatigations  and come up with diagnosis, treatment plan

.
 Entire real patient  clinical problem in this link here: //srianugna.blogspot.com/2020/05/hello-everyone.html

A 18 years old male patient with bilateral lower limb weakness since 20 days   the weak ness was started 2 years  back in proximal region  and gradually progressive to distal region.  bilateral  non pitting type of edema in lower limbs. H/o difficulty of squatting position and getting from the position. On examination there is areflexia.

 Weakness cause may be neuro genic , myogenic, traumatic cause .

No h/o trauma so it is ruled out.
 Neurogenic may be UMN LESION, LMN LESION. But the features are some related to LMN.

LOWER MOTOR LESION:
Anterior horn cells
Nerve roots
Peripheral nerves
Neuromuscular junction
Muscle

Anterior horn cells: it includes spinal muscular atrophy( areflexia, weakness,muscle twitching respiratory muscle involvement should be seen .diagnosis by genetic testing,  CT , MRI .By features , investigations it is ruled out.Nerve root( radiculopathies): there should be pain, radiation of pain diagnosis by CT , MRI. By above things we can rule out .

 Peripheral nerve involvement ruled out by nerve conduction studies,.

 Neuromuscular junction  -by features and  electromyography it can be ruled out from other diseases.

 Muscle(myogenic causes):  It may  include
Inflammatory causes- muscle biopsy is done and impression given-no suggestive of polymyositis.

Metabolic causes -no features of glycogen storage disorders.

Drug induced-no history of drug intake.
Endocrine causes-thyroid profile is normal thyroid myopathy is ruled out.

Diagnosis may be muscular dystrophy  (muscle biopsy)
Muscular dystrophy:
-myotonic dystrophy
- duchene's muscular dystrophy
--Beckers muscular dystrophy

Myotonic dystrophy :it involves facial muscle by sparing proximal muscles so it is ruled out.

Duchenes muscular dystrophy, beckers muscular dystrophy are genetic disorders but  patient with DMD will occurs symptoms by 3 to 5 years of age and may die by 18 to 20 years  with lung infections joint contractures, but in beckers disease there weakness,  proximal muscles are involved but onset of symptoms take longer time, there will be hypertrophy of calf muscles.

Investigations:
 Genetic  testing - mutation of DMD gene
Electromyography- to differentiate between muscle or nerve causes.

 Renal function tests-creatinine , urea levels are more, levels of phosphorous , calcium, potassium levels are taken to rule out rhabdomyolysis.

Complete urine examination is done

ECG -ventricular hypertrophy (cardiomyopathy)
 The diagnosis may be BECKER'S MUSCULAR build DYSTROPHY.

ANATOMICAL SITE-MUSCLE

 PHYSIOLOGICAL DISABILITY-difficult to squat and change the position from squatting to standing, to climb upstairs, wearing of slippers.

TREATMENT: no cure for this beckers disease yet. Symptomatic treatment,  steroids are given to slow down the progression,  prednisone may helpful in production of utrophin which closely ressembles dystrophin. Orthopaedic surgeons can treat  contractures,  associated with cardiomyopathy can be treated by ACE inhibitors, ARBS,beta blockers.

 Non pharmacologically  -physiotherapy, rehabilitation

A case of 18 yr old male patient with bilateral lower limb weakness since one month

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 .

      

A CASE OF A 42 YEAR OLD WOMAN WITH MULTIPLE HEALTH EVENTS SINCE BIRTH

D. Arun Kumar

Roll no: 46

I have 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 comeup with a diagnosis and  treatment plan.

You can find the entire real patient clinical problem in this link here: (https://classworkdecjan.blogspot.com/2019/05/42-f-with-severe-regular-edema-with_17.html?m=1 )

Following is my analysis of this patients problem : 

1. Frequent falls to the left with loss of function of the left side of the face and limbs. Complaint of a broken ankle after a fall from the staircase.

2. High salt intake  i.e about 2 to 4 tablespoons per day. 

3. Easy fatiguability with poor stress response

4. Fluctuating edema and alopecia.

 

And the reason for the problem may be: 

1. With respect to the frequent falls to the left and loss of function and sensations of the left side of face and limbs  the cause cannot be known. This may be due to raised ICP or any space occupying lesions in the brain which may give rise to migraines with cluster headache and  transient balckouts.

The investigation I suggest is fundoscopy to rule out any signs of raised ICP and a lumbar puncture. MRI to rule of any space occupying lesions.

2. The patient tells us that high salt intake helps her when she is sick and she feels more salt is needed when she feels sick. There is evidence of connection between the increased salt intake with lower stress rates according to the research done  at the University of haifia , department of psychology based on the study done on rats . Their blood pressure and heart rate didn't go up in response to stress  and to explain their findings they theorized that aldosterone and glucocorticoids which are released act on kidney and cause  dehydration also act on brain  to regulate responsiveness to stressors. Thus this explains the  decrease of fatiguability during sick after salt intake and the likely cause of dehydration and decreased sweating. But increased salt i.e sodium intake should cause increased blood pressure especially if potassium is not consumed in equal amount and the patient may be getting her potassium from the apple she eats everyday( 150mg of k+ in  one small apple)

3. Easy fatiguability is due to hemolytic anaemia which is due to G6PD deficiency.  This is already a proven fact that the patient has  G6PD deficiency and AMPD1 deficiency. AMPD1 deficiency leads to decreased atp production so easy fatiguability. AMPD1 deficiency also causes decreased sleep.

4. Fluctuating edema is most commonly due to intake of foods or medications which have oxidants like  menthol, fava beans etc and due to medications like anti malarials. 

The patient is recommended to not consume these food items or medications.

Alopecia may be an auto immune condition.

Investigation: full genome sequencing should be done.

Treatment:

-Avoid triggers like oxidants 

-If Hemolytic episode is seen then hydration +blood transfusion based on severity of anemia.

Some of the treatment options:

1.Ribose diet and keto diet
2.L serine for sleep
3.cutting oxidative stress 
4.vitamin B complex
5.antioxidant vitamins
6.fructose+antioxdants 

References: 

-Wikipedia ( saltstick.com/2017/11/27/stress-and-salt-intake) and ( https://healthfully.com/salt-anxiety-6389233.html ) 

-Dr.Avinash  Kumar's blog.