Tuesday, 8 September 2020

Case study of 45 yr old female pt. With anasarca

 

Analysis on 45year old female patient with anasarca.      




D. Arun Kumar
Roll no: 46

   I have been given this case in an attempt to solve in attempt to understand the patient's clinical data analysis to develop my competency in reading and comprehending including history, clinical findings, examination, investigations, and plan of treatment 


The complete details of the patient's history https://alekyatummala.blogspot.com/2020/09/45-yr-female-with-anasarca.html?m=1 are given this case

The main complaints of the patient are -

1. Pedal edema pitting type
2. Generalized edema
3. Shortness of breath at rest (NYHA grade 4)
4. Chest pain on the right side
5. Anuria 

Causes of Generalized Edema - Differential Diagnosis Algorithm Overfill  (Increased renal sodium retention,

Causes of generalized edema :

1.Heart failure 
2.cirrhosis of liver
3.kidney disease
4.hypoalbuminemia
5. Drug-induced edema
6. nutritional origin









what is the anatomical and etiological diagnosis of the patient :


anatomical diagnosis- kidney injury
etiological diagnosis-nephropathy due to diabetes, hypertension


what are the reasons for :

azotemia is a medical condition characterized by abnormally high levels of nitrogen-containing compounds (such as ureacreatinine, various body waste compounds, and other nitrogen-rich compounds) in the blood. It is largely related to insufficient or dysfunctional filtering of blood by the kidneys.
 It can lead to uremia and acute kidney injury (kidney failure) if not controlled.







Postrenal azotemia

ANEMIA - the kidney's function is to produce adequate amount of erythropoietin , when there is kidney damage these levels are reduced thereby causing anemia ( relative deficiency of erythropoeitin )
other causes include :
  • diminished red blood cell survival
  • iron deficiency due to loss of appetite and malnutrition
  • folate or vitamin b12 deficiency 
3. HYPOALBUMINEMIA -  due to excessive loss of proteins in urine and increased proximal tubule catabolism of filtered albumin .edema results from sodium retention and reduced plasma oncotic pressure which favors fluid movement from capillaries into the interstitium .to compensate for the perceived decrease in effective intravascular volume activation of RAAS, stimulation of AVP and activation of the sympathetic nervous system takes place, promoting continued salt and water reabsorption and progressive edema 

4 ACIDOSIS - normally kidneys maintain acid-base regulation, which when disturbed due to any kidney disorder causes metabolic acidosis . in this patient ph = 7.19 and reduced bicarbonate levels of 6.7 mmol/l which indicates metabolic acidosis .it occurs because of :
  • increase in endogenous production of acid (such as lactate or ketoacidosis )
  • loss of bicarbonate levels 
  • accumulation of endogenous acids because of inappropriately low excretion of net acid by the kidney ( as in CKD ) 
In this patient, it is due to the accumulation of endogenous acids due to inappropriate excretion by the kidney 

what is the rationale of her treatment plan detailed day-wise in the record ?

On day 1 :

1.Inj. NaHCO3 is given in order to neutralize the acidosis 
EFFICACY  -
 treat acidosis with ventilation and perfusion  by increasing plasma bicarbonate, buffers excess hydrogen ions and raises blood ph, and reverses clinical manifestations caused by acidosis 
also thought to worsen heart conditions and liver functions 

INDICATIONS OF IV SODIUM BICARBONATE : 
  • TO treat metabolic acidosis when the underlying disease is diarrhea, vomiting, or kidney-related diseases 
  • high blood potassium 
  • tricyclic anti-depressant overdose 
  • cocaine toxicity 
CONTRAINDICATIONS :
  • contraindicated in patients who are losing chloride 
  • it should be used with great care in patients of  CCF, severe CKD  due to its sodium content because in these conditions sodium retention is a problem 
  • it should be given in patients using corticosteroids with caution 
USES OF ORAL SODIUM BICARBONATE ARE :
  • as an antacid to treat heartburns, indigestion, upset stomach 
 WHY CONTRAINDICATED :
  • Hypersensitivity 
  • metabolic/respiratory alkalosis and hypocalcemia - because alkalosis produces tetany 
2. POTCHLOR syrup is given to correct hypokalemia 
3. ORAL HYPOGLYCEMIC AGENTS - used as a diabetic agent to lower glucose levels in the blood 
4. ANTI HYPERTENSIVES - to treat hypertension (to lower blood pressure value)

On day 2 :

1. Inj.HAI - used in type2 diabetes patients when their meat plan, weight loss, exercise, and antidiabetic drugs do not achieve targeted blood sugar levels 
2. orofer - for treatment of iron and folic acid deficiency i.e anemia 
3.PAN -Treatment of conditions due to excess acid secretion in the digestive system 
4. LASIX - a diuretic which is used to reduce the risk of strokes, heart attacks, and kidney problems 
contraindications are :
  • kidney disease 
  • hypokalemia 
  • diabetes - when taken furosemide it is hard to control blood sugar levels 
  • liver disease 

On day 3

1.tab Dytor - given to control fluid overload and blood pressure since the patient had higher blood pressure on day 3
2.telma - Telmisartan is given to treat hypertension, heart failure and diabetic kidney disease .may be because of its limitation that it reduces the amount of urine and increases kidney damage it could be stopped
3. Nicardia is given to lower blood pressure 
4.Orofer  and erythropoietin inj- in order to correct anemia and increase levels of erythropoietin which further corrects anemia
5. Shelcal - it is given to treat hypocalcemia 
6. Potchlor syrup - to correct hypokalemia 
7.nodosis - it is an antacid, to neutralize the excess acid present in the stomach

On day 4:

1. Lactulose - since the patient complained she had constipation she was given lactulose after which she passed the stools
2.inj.monocef- it is an antibiotic. Used to treat UTI or any other infections  
3. Protein x powder -  given since the patient is malnourished 
but excess use can cause coma, hepatic damage, metabolic disturbances, unpleasant taste in the mouth

On day 5 

The patient was further evaluated to improve her condition 

what was the indication for dialyzing her and what was the crucial factor that led to the decision to dialyze her on the 3rd day of admission? 

  • severe breathlessness due to pulmonary edema 
  •  acid-base problems ( METABOLIC ACIDOSIS )
  • pericarditis 
  • electrolyte imbalance 

On 3rd day of her admission, the crucial factor that led to the decision to dialyze her was due to - FLUID OVERLOAD / PULMONARY EDEMA REFRACTORY TO DIURETICS  and Refractory anuria

what are the other factors other than diabetes and hypertension that led to her current condition?

 it may be due to anemia, vascular disease, and constipation 

what are the expected outcomes in this patient? Compare the outcomes of similar patients globally and share your summary with reference links?

as mentioned in the above link : 
 chronic pressure overload, progressive volume overload, cardiomyopathy  with the additional risk factor of Diabetes, Anemia could lead to preserved LVEF / reduced LVEF which further lead to the outcome of :
  • Progression of CKD 
  • HF hospitalization
  • Sudden arrhythmic death
  • Pump failure of death

How and when would you evaluate her further for cardio-renal HFpEF and what are the mechanisms of HFpEF in diabetic renal failure patients?

Evaluation for HFpEF must be done on the day of admission itself if there is suspicion of heart-related disorder such as heart failure as per the patient's symptoms, clinical examination, and laboratory diagnosis 
Evaluation for cardio-renal HEpEF :
  • Echocardiography - provides information on chamber volumes, ventricular systolic and diastolic dysfunction, wall thickness, valve function, and filling pressures 
  • Chest radiography - to screen for other sources of dyspnea 
  • Electrocardiography - to detect rhythm disturbances or evidence of prior myocardial damage or pericardial disease 
  • MRI 
  • global longitudinal strain analysis 
  • whole -body bioimpedance technique 
  • extended cardiac rhythm monitoring 
Emerging diagnostic options include :
  • Pulmonary artery ambulatory monitoring 
  • thoracic impedance monitoring 
decreased renal blood flow leads to the stimulation of the RAAS mechanism resulting in :
  •  sodium, water retention leading to volume overload thereby increasing blood pressure and cardiac work, myocardial fibrosis finally causing heart failure 
  • leads to vasoconstriction leading to increased afterload, increased  blood pressure, leading to heart failure

 What are the efficacies over placebo for the available therapeutic options being provided to her for her anemia? 

referred link as follows

https://pubmed.ncbi.nlm.nih.gov/19245362/

https://clinicaltrials.gov/ct2/show/NCT01114139

What is the utility of tools like the CKD-AQ that assess the frequency, severity, and impact on daily activities of symptoms of anemia of CKD? Is Telegu among the 68 languages in which it is translated? 

CKD-AQ - about frequency, severity of symptoms, signs associated with anemia.


https://academic.oup.com/ckj/advance-article/doi/10.1093/ckj/sfz091/554348
https://www.smartpatients.com/trials/NCT034091072

what is the contribution of PEM to her severe hypoalbuminemia? what is the utility of tools such as SGA( subjective global  assessment ) in the evaluation of malnutrition in CRF patients

 Nutritional deficiencies particularly that of iron and zinc and decreased supply of amino acids to the liver causes reduced production of albumin levels thus leading to hypoalbuminemia 

Nutritional status as determined by Subjective Global Assessment -Dialysis Malnutrition Score is a useful and reliable index for identifying patients at risk for malnutrition and it correlates well with the anthropometric and biochemical assessment. May be integrated into the regular assessment of malnutrition in patients on maintenance hemodialysis
Differences in the diagnosis of a 45-year-old female and a 58-year-old man ; 
As per the clinical findings of the patient of 45-year-old 
  • Albuminuria
  • decreased urine output 
  • Abnormal renal biopsy
  • on USG - loss of CMD and increased echogenicity
  • Hence could be diagnosed as CKD due to diabetic nephropathy
As per 58-year-old male patient:
  • Increased bun/serum creatinine >20:1 which may indicate AKI
  • Low urinary output 
  • Flank pain
  • On USG - there's no increase in echogenicity and other abnormality is not detected  and left kidney size reduced 
  • Hence could be diagnosed as AKI  

Differences in management:

45-year-old patient :
  • Potchlor was given to correct hypokalemia
  • shelcal for hypocalcemia 
  • Lasix to correct fluid overload
  • anti-diabetic and antihypertensive agents are given 
  • further investigations are done to improve the patient condition 
58-year-old patient :
  • Piptaz - an antibiotic 
  • Amlong tablet - for treatment of hypertension 
  • Lasix to combat fluid overload
  • Pantop - an antacid
  • HAI - to reduce blood sugar levels

Differences in outcomes 

in AKI :
In CKD :

Would you agree with the provisional diagnosis of a 58-year male patient as per the online case report? 

Yes I would agree with the provisional diagnosis that is AKI since the patient has bun/creatinine ratios increased >20:1 and he complained of burning micturition, hyponatremia (mild) 

References :

1.Dr.Alekya Reddy mam's blog 
2. Dr.Bhavya mam's blog 
3.Harrison's book of medicine
4.all the links shared at their respective texts


Saturday, 23 May 2020

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 .
      

Saturday, 16 May 2020

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.