Heart failure case 2

G Kusuma 

58 

I am final year student taking part in active learning in solving case given to me in the following link

https://himabindu5.blogspot.com/2020/05/hello-everyone.html

Cheif complaints 

• Chest pain since 2 months
• Palpitation since 2 montha
• Dyspnea
• Bilateral pedal edema extending till ankle
• Decreased urine output

Chest pain

> towards left

> more in epigastric region

>non radiating 

Is it cardiopulmonary or non cardiac causes lead too chest pain ???? Was my first question

For that major causes of chest pain should be aligned 

Interpretation from above causes

Cardiac: acute caronary mainly MI

Troponin is negative so cant be MI

 , pericarditis, myocarditis since this are sudden acute in onset can be ruled out and mainly no history of fever seen

Non cardiac causes no history is suggestive of non cardiac causes so i rule out 

Probability of valvular disease is still a question which should be confirmed 

It might also be anemia or thyroid dysfunction 

Palpitations 

What made the person to palpate ....????

What investigation done to patient suggestive or localise palpitation???

• What about pulse 

Feeble  , irregularly iregular

• Ecg??

Irregular rythm P wave absent  indicating atrial 

Right axisis deviation indicating enlarged heart

St elevation in v4 v5 aVR

Jvp was raised and showed prominent a wave 

What is the correlation of atrial contraction abnormality & DYSPNEA , PEDAL EDEMA , DECREASED URINE OUT PUT ?????

So the pulmonary edema might be resulting in dyspnea 

Orthopnea

Decreased urine out put might be due to decreased blood flow to kidney asa compensation of decreased activity of the heart which also explains pedal edema 

Other investigation 

On Auscultation,

                                Mitral area: Loud S1 heard

                                Tricuspid area: Loud S1 heard

                                Pulmonary area: Splitting of S2-loud P2 component

                -On X-ray imaging: Cardiomegaly - Enlargement of Rt. Atrium, Rt. Ventricle, Lt. Ventricle

                -In 2D echo, Mitral valves calcification and fish mouth appearance was seen 

Provisional diagnosis : Mitral valve stenosis with heart failure 

Treatment

If you have mild to moderate mitral valve stenosis with no symptoms, you might not need immediate treatment. Instead, your doctor will monitor the valve to see if your condition worsens.

Medications

No medications can correct a mitral valve defect. However, certain drugs can reduce symptoms by easing your heart's workload and regulating its rhythm.

Your doctor might prescribe one or more of the following medications:

Diuretics to reduce fluid accumulation in your lungs or elsewhere.

Blood thinners (anticoagulants) to help prevent blood clots. A daily aspirin may be included.

Beta blockers or calcium channel blockers to slow your heart rate and allow your heart to fill more effectively.

Anti-arrhythmics to treat atrial fibrillation or other rhythm disturbances associated with mitral valve stenosis.

Antibiotics to prevent a recurrence of rheumatic fever if that's what caused your mitral stenosis.

Procedures

You may need valve repair or replacement to treat mitral valve stenosis, which may include surgical and nonsurgical options.

Percutaneous balloon mitral valvuloplasty

In this procedure, also called balloon valvotomy, a doctor inserts a soft, thin tube (catheter) tipped with a balloon in an artery in your arm or groin and guides it to the narrowed valve. Once in position, the balloon is inflated to widen the valve, improving blood flow. The balloon is then deflated, and the catheter with balloon is removed.

For some people, balloon valvuloplasty can relieve the signs and symptoms of mitral valve stenosis. However, you may need additional procedures to treat the narrowed valve over time.

Not everyone with mitral valve stenosis is a candidate for balloon valvuloplasty. Talk to your doctor to decide whether it's an option for you.

Mitral valve surgery

Surgical options include:

Commissurotomy. If balloon valvuloplasty isn't an option, a cardiac surgeon might perform open-heart surgery to remove calcium deposits and other scar tissue to clear the valve passageway. Open commissurotomy requires that you be put on a heart-lung bypass machine during the surgery. You may need the procedure repeated if your mitral valve stenosis redevelops.

Mitral valve replacement. If the mitral valve can't be repaired, surgeons may perform mitral valve replacement. In mitral valve replacement, your surgeon removes the damaged valve and replaces it with a mechanical valve or a valve made from cow, pig or human heart tissue (biological tissue valve).

Biological tissue valves degenerate over time, and often eventually need to be replaced. People with mechanical valves will need to take blood-thinning medications for life to prevent blood clots. Your doctor will discuss with you the benefits and risks of each type of valve and discuss which valve may be appropriate for you.

Fever leading to heart failure .....

G Kusuma
58
Studying Final year part 2 ....

I was given a case of 35 year male  and details were given in the following link 

https://madhur116.blogspot.com/2020/05/on-1452020.html?m=1

Cheif complaints 

Asymptotic 1 month back than developed fever of high grade

Associated with  chills 

Causes:

• Bacterial
• Parasitic
• Viral

Antimalaria medication was given but fever subsided spontaneously and characteristic of high grade indicating...... most propably viral cause ....

2. Pedal edema  

Bilateral  , pitting type 

Causes

• Cardiac failure
• Liver failure
• Renal failure 
• Drug causes
• Dvt

I conclude cause for edema to CARDIAC  causes since history 

doesn’t support dvt 

Drug causes since no history related to drug usage

Renal causes since no periorbital edema or oliguria seen

Liver causes since no bilirubin variation or ascitis seen

3. Dyspnea

Initally NYHA classification 3 

On medication decreased to class 2

Paroxymal nocturnal dyspnea

Why dyspnea ..????

What exactly happened to his heart???

Examination findings

Genreal examination show normal finding

CNS :  intact 

            Motor system normal

            Sensory system normal

            No cerebral signs

Cvs : s1 s2  heard normal

Early inspiratory crepts heard which make diagnosis confined to heart 

Jvp raised  elevated a wave indicating Tricuspid regurgitation

USG : shows moderate pleural effusion with ascites 

            Grade 1 fatty liver 

https://drive.google.com/file/d/1K9Fk66l6c79ziOF-dIYQ3vDlGbSavlr7/view?usp=drivesdk

2D ECHO:EF-27%

                  IVC dilated(2.3cm)not collapsing.   Due to dialation of ivc blood back flow

                  mild TR+    Due to valvular dysfunction

                  severe MR+    Due to valvular dysfunction

                  trivial AR+     Due to valvular dysfunction

                  dilated all chambers 

                  global hypokinesia. Due to cardiomegaly

                  severe LV dysfunction due to valvular dysfunction 

                  mild PAHT

                  no MS/AS

                  no PE/LV clot

  What happened to valves ?? 

Case history shows valvular dysfunction 

                             👇🏻👇🏻

           which is the reason for obstruction  

                              👇🏻👇🏻

             Heart load increases

                               👇🏻👇🏻

              Remodeling of heart tissue leads to cardiomegaly 

                               👇🏻👇🏻

           Leads to regurgitaion of blood to IVC , Pulmonary veins 

                               👇🏻👇🏻

            Ivc regurgitation leads to portal hypertension liver dysfunction 

            Backward flow of blood to lungs lead to acumulation of fluids and dyspnea 

                                 👇🏻👇🏻

                Heart failure 

                             

  What lead to valvular dysfunction..?

In my interpretation valvular dysfunction in my case might be due to viral fever mostly coxsackie virus  which mimics molecular resembles heart molecules and cause MYOCARDITIS
which lead to all the other symptoms  and heart failure

Provisional diagnosis      : heart failure with reduced ejection fraction secondary to viral myocarditis or inflammatory myocarditis 

Further investigations i suggest 

Cardiac catheterization and endomyocardial biopsy. A small tube (catheter) is inserted into a vein in your leg or neck and threaded into your heart. In some cases, doctors use a special instrument to remove a tiny sample of heart muscle tissue (biopsy) for analysis in the lab to check for inflammation or infection.

Treatment 

In many cases, myocarditis improves on its own or with treatment, leading to a complete recovery. Myocarditis treatment focuses on the cause and the symptoms, such as heart failure.

In mild cases, persons should avoid competitive sports for at least three to six months. Rest and medication to help your body fight off the infection causing myocarditis might be all you need. Although antiviral medications are available, they haven't proved effective in the treatment of most cases of myocarditis.

Certain rare types of viral myocarditis, such as giant cell and eosinophilic myocarditis, respond to corticosteroids or other medications to suppress your immune system. In some cases caused by chronic illnesses, such as lupus, treatment is directed at the underlying disease.

Drugs to help your heart

If myocarditis is causing heart failure or arrhythmias, your doctor might hospitalize you and prescribe drugs or other treatments. For certain abnormal heart rhythms or severe heart failure, you may be given medications to reduce the risk of blood clots forming in your heart.

If your heart is weak, your doctor might prescribe medications to reduce your heart's workload or help you eliminate excess fluid, including:

Angiotensin-converting enzyme (ACE) inhibitors. These medications, such as enalapril (Vasotec), captopril (Capoten), lisinopril (Zestril, Prinivil) and ramipril (Altace), relax the blood vessels in your heart and help blood flow more easily.

Angiotensin II receptor blockers (ARBs). These medications, such as losartan (Cozaar) and valsartan (Diovan), relax the blood vessels in your heart and help blood flow more easily.

Beta blockers. Beta blockers, such as metoprolol (Lopressor, Toprol-XL), bisoprolol and carvedilol (Coreg), work in multiple ways to treat heart failure and help control arrhythmias.

Diuretics. These medications, such as furosemide (Lasix), relieve sodium and fluid retention.

Treating severe cases

In some severe cases of myocarditis, aggressive treatment might include:

Intravenous (IV) medications. These might improve the heart-pumping function more quickly.

Ventricular assist devices. Ventricular assist devices (VADs) are mechanical pumps that help pump blood from the lower chambers of your heart (the ventricles) to the rest of your body. VADs are used in people who have weakened hearts or heart failure. This treatment may be used to allow the heart to recover or while waiting for other treatments, such as a heart transplant.

Intra-aortic balloon pump. Doctors insert a thin tube (catheter) in a blood vessel in your leg and guide it to your heart using X-ray imaging. Doctors place a balloon attached to the end of the catheter in the main artery leading out to the body from the heart (aorta). As the balloon inflates and deflates, it helps to increase blood flow and decrease the workload on the heart.

Extracorporeal membrane oxygenation (ECMO). With severe heart failure, this device can provide oxygen to the body. When blood is removed from the body, it passes through a special membrane in the ECMO machine that removes carbon dioxide and adds oxygen to the blood. The newly oxygenated blood is then returned to the body.

The ECMO machine takes over the work of the heart. This treatment may be used to allow the heart to recover or while waiting for other treatments, such as a heart transplant.

In the most severe cases, doctors might consider urgent heart transplantation.

Some people might have chronic and irreversible damage to the heart muscle requiring lifelong medications, while other people need medications for just a few months and then recover completely. Either way, your doctor is likely to recommend regular follow-up appointments, including tests to evaluate your condition.

 
Refrence from

https://www.mayoclinic.org/diseases-conditions/myocarditis/symptoms-causes/syc-20352539

Paraparesis case 2

G Kusuma
58
I was given a case of Paraparesis
https://hitesh116.blogspot.com/2020/05/elog-13th-may-2020.html?m=1

  

Cheif complaints

• Difficulty in climbing stairs since one month
• Bilateral lower limb weakness since one month
• Difficulty in holding cheppal
• Wasting and thinning of lower limb muscles more than upper limb
• No history showing sensory involvement 
• No history showing involuntary movements 
• Cerebral invovment based history was not there

So my diffrentials concised to UMN or LMN lesions 

On examination

On examination we find

Normal grneral examination

Hemogram , serum electrolysis , other lab investigations wer normal

Thyroid tests were normal 

CNS examination showed

1. Atophy
2. Hypotonia
3. Absent deep tendon reflex
4. Babinski sign negative 

This confines my diagnosis to LMN lesion

Lesion of LMN can be located at four places on its pathway

Anterior horn cell

Peripheral nerve

NMJ

Muscle (myopathy)

To rule out Anterior horn cell disease and peripheral neuropathy , evaluation of conduction velocity (NCV), histological findings , biochemical studies are necessary. 

NCV testing has to be done in the patient , which helps us to know whether it is neurogenic.

ELECTROMYOGRAPHY is done and showing normal results , from which we can rule out NMJ disorders.

Since in case motorin involvment is predominantly seen

Diagnose confined to 

Myopathy

Peripheral neuropathy 

To specify
As they wer conducted thyroid tests and wer normal HYPOTHYROIDISM can be ruled out
So being myopathy is highly not possible 
Might be 
Peripheral neuropathy 

Treatment 

Effective prognosis and treatment of peripheral neuropathy relies heavily on the cause of the nerve damage. For example, a peripheral neuropathy caused by a vitamin deficiency can be treated -- even reversed -- with vitamin therapy and an improved diet. Likewise, nerve damage brought on by alcohol abuse can often be stopped and improved by avoiding alcohol. Peripheral neuropathy caused by toxic substances or medications can often be corrected in much the same way. When neuropathy is related to diabetes, careful monitoring of blood sugar levels may slow its progression and curb symptoms.

Early diagnosis and treatment of peripheral neuropathy is important, because the peripheral nerves have a limited capacity to regenerate, and treatment may only stop the progression -- not reverse damage. If you have become severely impaired, you may need physical therapy to help retain strength and avoid muscle cramping and spasms.

https://www.webmd.com/brain/understanding-peripheral-neuropathy-treatment

Paraparesis case 1

G Kusuma

58 

I was given a case of Paraparesis 

https://srianugna.blogspot.com/2020/05/hello-everyone.html

Cheif complaints 

Bilateral lower limb weakness since 20 days 

Started proximal later progressed to bilateral distal region

Bilateral edema which is non pitting 

Difficulty in squatting and getting up

Difficulty in wearing chepals

NO H/O DIFFICULTY IN COMBING HAIR , BUTTONING AND UNBUTTONING SHIRT

NO H/O CRANIAL NERVE INVOLVEMENT

                       Neurological weakness

1. Upper motor neuron

2. Basal ganglia and cerebellum

3. Lower motor neurons

 Other causes of weakness might be 

Systemic 

Drug induced

Vitamin deficiency 

Autoimmune diseases

Thyroid condition

On examination 

Patient is coherent conscious and cooperative 

 general examination was normal

Higher mental status is normal

Cranial nerve functions are intact

Motor system

Tone normal

Power slightly decreased 4/5 in both lower limb

Reflexes are absent in both lower limbs

Sensory system was intact 

No specific signs of meninges or cerebellar

Lab investigation 

Blood 

Urine 

Ecg

Serology

All were normal with minor variabilities

Muscle biopsy done Not suggestive of polymylities or muscular dystrophy 

Probable localisation and ruling out

Upper motor neuron lesion

From cerebral cortex to spinal cord 

Symptoms of UMN lesion

Distal muscle involvement mostly

Hypertonia

Flexor weakness

Deep tendon reflexes are exaggerated 

But our case show none so can rule out UMN lesion

Cerebellum

Dysdiadokinesis 

Gait abnormality 

Hyponia

Dysarthria

Nystagmus 

Intesion tremors

Pendular knee jerk

This were not related soo cerebral lesions wer highly imposible

Lower motor neuron lesion 

mostly proximal muscle are involved

atrophy of mucles

flaccidity

hypotonia

deep tendon reflexes are reduced or absent

babinski is negative

fasiculations and fibrillations are present

Lesion of LMN can be at four places on its pathway

Anterior horn cell

Peripheral nerve

NMJ

Muscle (myopathy)

To rule out Anterior horn cell disease and peripheral neuropathy , evaluation of conduction velocity (NCV), histological findings , biochemical studies are necessary. 

NCV testing has to be done in the patient , which helps us to know whether it is neurogenic.

ELECTROMYOGRAPHY is done and showing normal results , from which we can rule out NMJ disorders.

It might not be drug induced no suggestive history of medication

Hypothyroidism can be ruled out by thyroid harmone status

No relapsing events so chronic demyelination polyneuropathy can be ruled out

Muscular dystrophy was ruled out by histopathology report

Case might most probably be BECKER’s Muscular dystrophy which is a X linked recessive trait

Becker Muscular Dystrophy (BMD) is an inherited disorder of muscle structure that results in progressive weakness of limb and breathing muscles. The involuntary muscles are not affected. BMD is similar to Duchenne Muscular Dystrophy (DMD), but is less severe. BMD usually begins in the teens or early adulthood, and the course is slower and far less predictable than that of DMD. Early symptoms are cramps after exercising, and later in life the person begins to experience problems while walking quickly or running. Other noticeable symptoms besides weakness are falling, feeling "worn out," and changes in the skeletal system. Few affected have learning problems, but these cases are typically minor.

What causes Becker Muscular Dystrophy?

The cause of BMD is related to a deformity of a gene on the X chromosome (therefore, females are the carriers of this defect). This fault produces a protein called dystrophia that does not work the way it should within muscle fibers. This causes the fibers to gradually weaken and wear away.

Who gets Becker Muscular Dystrophy?

Boys are affected almost exclusively and every ethnic background is affected. In a group of 100,000 people, approximately 3 will be affected with BMD Some patients who have BMD can live a normal lifespan, however most die sometime after the age of 40.

How is Becker Muscular Dystrophy diagnosed?

BMD can often be misdiagnosed as limb-girdle muscular dystrophy or as spinal muscular dystrophy. Blood tests can be performed if it is known that BMD runs in the family. Needle EMGs and nerve conduction studies (NCSs) can also be performed. The needle EMG will show that the muscle weakness is due to a problem with the muscles versus problems with nerves.

How is Becker Muscular Dystrophy treated?

The treatment of BMD focuses on lessening the symptoms associated with it. There is no cure, but treatments are available to help with symptoms and maximize muscle function. It is vital that a person with BMD stay in shape and continue to use their muscles. This can include physical therapy. Treatment can also include genetic counseling, using splints, massages, and catabolic steroids. It is probable that the person will eventually require a wheelchair.

Information Taken from

https://www.aanem.org/Patients/Muscle-and-Nerve-Disorders/Becker-Muscular-Dystrophy