TEP repair for Inguinal Hernia, No Balloon dissector, No fixation Tacks, Dr. AKshay Bahadur

 

Difficult Laparoscopic Cholecystectomy with repair of Cholecysto-gastric Fistula

Inguinal Hernia Repair: Total Extraperitoneal

Laparoscopic Appendectomy

Interval laparoscopic appendectomy in a 18 year old girl.

Open cholecystectomy, Learn simple and safe technique

Laparoscopic Cholecystectomy

Laparoscopic Cholecystectomy is safe if the Critical View of Safety (CVS) method of identification of the cystic duct and cystic artery is performed wherever possible. As per SAGES, three criteria are required to achieve the CVS:
1. The hepatocystic triangle is cleared of peritoneum, fat and fibrous tissue. The hepatocystic triangle is defined as the triangle formed by the cystic duct, the common hepatic duct, and inferior edge of the liver. The common bile duct and common hepatic duct do not have to be exposed.
2. The lower one third of the gallbladder is separated from the liver to expose the cystic plate. The cystic plate is also known as liver bed of the gallbladder and lies in the gallbladder fossa.
3. Two and only two structures should be seen entering the gallbladder.

Open cholecystectomy with Cholecystogastric fistula

Open Cholecystectomy in a complicated case of Cholecystogastric fistula with minimum instruments, moderate incision, No Sandbag at back, No Sponge on Holder, No Pea-nut on holder, No blunt dissection with almost negligible bleeding in quick time under spinal anesthesia in a 45 year old female GA unfit patient is "POSSIBLE".

Open Cholecystectomy

Laparoscopic Total Extraperitoneal (TEP) Repair Lt Direct inguinal Hernia

Laparoscopic Total Extraperitoneal (TEP) Repair Lt Direct inguinal Hernia

Laparoscopic Total Extraperitoneal (TEP) Repair of Left Direct Inguinal Hernia

Myocardial infarction (Heart Attack)

       Heart muscle is the hardest working muscle of the body which pumps approximately 4-5 litre of blood ever minute during rest. Only coronary arteries supply blood to heart muscle. Blood flowing through the chambers of the heart is not useful for the heart muscle.

Heart attack or Myocardial infarction (MI) is the irreversible necrosis (death) of heart muscle secondary to prolonged ischemia (lack of oxygen supply). This usually is the result of a blockage in one or more of the coronary arteries. During last 30 years, large decline of MI incidence in developed countries and alarming increase in developing countries like India.

Etiology

Atherosclerosis: Atherosclerosis is a condition in which there is gradual plaque build-up within artery walls, resulting in narrowing of artery. Atherosclerosis is the disease primarily responsible for most acute coronary syndrome (ACS) cases.

Coronary artery disease (CAD) or Coronary heart disease (CHD): when atherosclerosis occurs in coronary arteries, heart does not get sufficient blood, the condition called coronary artery disease or coronary heart disease.

Non-modifiable risk factors:

Ø  Age: Men are at a higher risk of heart attack after age 45 and women after age 55.

Ø  Family history: A positive family history of MI in first-degree male relative aged 45 years or younger and first-degree female relative aged 55 years or younger.

Ø  Male-pattern baldness.

Modifiable risk factors:

Ø  Smoking or other tobacco use.

Ø  Bad cholesterol (LDL), is one of the leading causes of a blockage in the arteries.

Ø  Saturated fats may also contribute to the build-up of plaque in the coronary arteries. Saturated fats are found mostly in meat and dairy products, including beef, butter, and cheese.

Ø  Trans fat contributes to clogging of arteries. Trans fat is usually artificially produced and can be found in a variety of processed foods.

Ø  Diabetes mellitus: High blood sugar levels can damage blood vessels and eventually lead to coronary artery disease.

Ø  Hypertension: High blood pressure damages arteries and accelerates the build-up of plaque.

Ø  Obesity (abdominal obesity)

Ø  Psychosocial stress

Ø  Sedentary lifestyle and/or lack of exercise

Ø  Reduced consumption of fruits and vegetables

Ø  Poor oral hygiene

Ø  Type A personality

Ø  Elevated homocysteine levels

Symptoms

Ø  Chest pain: The typical chest pain of acute MI usually is intense and unremitting for 30-60 minutes. It is retrosternal and often radiates up to the neck, shoulder, and jaws, and down to the left arm. The chest pain is also perceived as squeezing, aching, burning, or even sharp.

Ø  There may have prodromal symptoms of fatigue, chest discomfort, or malaise in the days preceding the event; alternatively, typical ST-elevation MI (STEMI) may occur suddenly without warning.

Ø  Profuse sweating.

Ø  Shortness of breath.

Ø  Anxiety, commonly described as a sense of impending doom.

Ø  Light headedness, with or without syncope.

Ø  Coughing, wheezing, and the production of frothy sputum may occur.

Ø  Nausea, with or without vomiting.

Ø  In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas.

Ø  Many Myocardial infarctions are either "silent" or are not clinically recognized by patients, families, and health care providers.

Signs

Ø  Tachycardia: The patient’s heart rate is often increased.

Ø  Irregular Pulse.

Ø  Blood Pressure: BP initially elevated because of peripheral arterial vasoconstriction. Later, with right ventricular MI or severe left ventricular dysfunction, there is hypotension (fall in BP) and cardiogenic shock can be seen.

Ø  Tachypnoea: The respiratory rate may be increased in response to pulmonary congestion or anxiety.

Investigations

Ø  Electrocardiography (ECG):

o   ECG is most important tool in the initial evaluation. ST-segment elevation greater than 1 mm in two anatomically contiguous leads or presence of new Q waves.

o   Intermediate-probability: ST-segment depression or T-wave inversion.

o   Low-probability: Normal ECG findings or nonspecific findings on ECGs do not exclude the possibility of MI.

Ø  Cardiac biomarkers/enzymes:

o   Cardiac troponin should be measured at presentation in suspected MI.

o   Troponin is a contractile protein that is not normally found in serum; it is released only when myocardial necrosis occurs.

o   Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days.

o   Serial measurement of cardiac troponins after the initial level is normal at presentation, 3 to 6 hours after symptom onset, is recommended.

Ø  Cardiac imaging:

o   Coronary angiography in individual with highly probable or confirmed acute MI can be used to definitively diagnose or rule out coronary artery disease.

o   Multi-detector computed tomography (MDCT) coronary angiography may be considered as an alternative to invasive angiography to exclude ACS when cardiac troponin and/or ECG results are inconclusive.

Prognosis

Ø  Acute myocardial infarction is associated with a 30% mortality rate; about 50% of the deaths occur prior to arrival at the hospital.

Ø  Approximately half of all patients with an MI are re-hospitalized within 1 year of their index event.

Ø  Better prognosis is associated with:

o   Successful early reperfusion (ST-elevation MI goals: patient arrival to fibrinolysis infusion within 30 minutes or percutaneous coronary intervention within 90 minutes.

o   Preserved left ventricular function.

o   Short-term and long-term treatment with beta-blockers, aspirin, and ACE inhibitors.

Ø  Poorer prognosis is associated with the following factors:

o   Advanced age.

o   Diabetes mellitus.

o   Previous cerebrovascular disease or peripheral vascular disease.

o   Delayed or unsuccessful reperfusion.

o   Poorly preserved left ventricular function.

o   Evidence of congestive heart failure.

o   Involvement of electrocardiograph (ECG) lead aVR.

o   Depression.

Management

Prehospital care

Ø  Intravenous access,

Ø  Supplemental oxygen if SaO₂ is less than 90% on pulse oximetry.

Ø  Aspirin: Aspirin preferably chewable should be given in a dose of at least 162 to 325 mg for fibrinolytic therapy, unless there is a clear history of aspirin allergy.

Ø  Nitroglycerin: Nitroglycerin 0.4 mg tablet sublingually or by spray should be given as it relaxes venous system reducing workload of the heart thereby help in chest pain. If relief is experienced within 5 minutes of the first Nitroglycerin dose, repeated doses can be given every 5 minutes for a maximum of 3 doses total.

Ø  Nitroglycerin should be avoided in hypotension or bradycardia.

Ø  Telemetry and prehospital ECG, if available

Ø  Adequate analgesia: Morphine in initial dose of morphine of 2 to 4 mg as an IV bolus can be given, repeated every 5 to 10 minutes until the pain is relieved.

Ø  The use of NSAIDs should be avoided as these are associated with adverse cardiovascular events.

Emergency department and inpatient care:

Ø  The first goal for healthcare professionals in management of acute myocardial infarction (MI) is to diagnose the condition in a very rapid manner.

Ø  Resuscitation of the patient.

Ø  Initial therapy is directed toward restoration of perfusion as soon as possible to salvage as much of the jeopardized myocardium as possible. This may be accomplished through medical or mechanical means, such as percutaneous coronary intervention (PCI), or coronary artery bypass graft (CABG) surgery.

Ø  Angioplasty (Percutaneous coronary intervention): A thin, flexible tube with a balloon on the end is threaded through a blood vessel to the blocked coronary artery. Then, the balloon is inflated to push the plaque against the wall of the artery. This widens the inside of the artery, restoring blood flow. Also a stent may be put in the artery to help keep it open.

Ø  Coronary artery bypass grafting (CABG): It is a surgery in which arteries or veins are taken from other areas of body and sewn in place to go around the blocked coronary arteries. This provides a new route for blood flow to the heart muscle.

Lifestyle modifications

Ø  Dietary changes: A low-fat and low-salt diet with dietary counseling,

Ø  Quit Smoking

Ø  Regular exercise: The recommended frequency of regular exercise training is three or more times a week, for at least 30 minutes per session.

Ø  Possible goal numbers for your risk factors include:

o   Blood pressure lower than 140/90 mm Hg

o   Waist circumference lower than 35” for women and 40” for men

o   Body mass index (BMI) between 18.5 and 24.9

o   Blood cholesterol under 180 mg/dL

o   Fasting Blood glucose under 100 mg/dl

Multiple Myeloma

Life Expectancy of Newly diagnosed Multiple Myeloma patient:

My family’s experience

Whenever a person, who in most instance otherwise looks healthy, diagnosed Multiple Myeloma, the first fearful question comes to mind is how long he/she will survive. Same question also came in my Brother’s mind who was just 48 when he was diagnosed for Multiple Myeloma. He was just having low backache, no other symptoms.

I sat by his side and he asked me: Bhaiya (Brother), everything is finished? As the articles on internet he read showed that he would not survive for more than 9 months. It was painful for both of us but being a doctor, I assured him that don’t go on what is written on net and we will fight and I will not let him go.

He was thoroughly investigated and the treatment started under the guidance of one of the finest Oncologist for Multiple Myeloma at AIIMS, Delhi. First chemotherapy and later autologous Stem Cell transplant, everything was going as planned. My brother was obese, moderate alcoholic and occasional smoker. He stopped these intoxications and started light exercise to reduce weight. He stuck to a healthy diet as prescribed to him.

Later, the symptoms gradually started subsiding, Hb% improving and so was other parameters. Every one of us including my brother started feeling relaxed, though we know that there will be relapse someday. We all forgot that the literature says life expectancy in current situation is 3 to 5 years. Gradually his daily routine started to what it was before the disease including diet, exercise and other habits.

Do we have to relax at this stage?

I still curse myself that being a doctor; it was my responsibility to tell my brother (who was not a medical professional) that the disease is still there in his body and that we cannot afford to relax. It was my duty to realize him that on first occasion his body able to bear the brunt of disease but next time when there will be relapse, the same body might not be in a stage to bear the injury. So this should be the time when we should be more focused to prepare a body system which is much fitter.

Since there is no cure of Multiple Myeloma till date, we should accept that the disease will take its own course. There may be complete remission followed by early or delayed relapse. We should be more focused especially in remission phase on how we can prepare our body to fight the relapse.

            If the patient has to live longer, if he has to erase the 3 years survival destiny, he has to continue all those instruction more stringently during remission phase, which was advised to him when he was first diagnosed the disease. Few of these are:

1.     No Alcohol: Better would be no addiction including smoking, chewing tobacco or Gutkha besides forgetting alcohol.

2.     No Obesity: Gradual but continuous reducing the weight with balanced diet and continuous exercise. It would be better if the patient do exercise under medical supervision as he has weak bones which are more prone to get damaged. The exercise should gradually be increased over a period.

3.     Strict diet Plan: A healthy diet keeping more of fruits, vegetables, proteins and less of carbohydrates, sugar, packed / processed foods.

4.     Develop Muscle Mass: I believe that the patient should gradually develop his/her muscles, especially of extremities / weight bearing areas.

5.     No shortcut treatment: There are many advertisements in which it is claimed that they can cure the patient. You may get many such examples. But believe me, all of them are fake and I am telling you from my personal experience.

Lastly, just leave the medical part on physician treating you but much more important is how you prepare your body against the disease.

Warning: The purpose of this article is to create awareness for the disease mentioned above. The reader of this article should exercise all precautions before following any information provided above and it is advised that you consult your own physician or other medical professional. The responsibility lies solely with the reader and not with the site or the writer.

Multiple myeloma

Dedicated to my Brother Sanjay Singh

Who left us for heaven on 22-11-2016 due to

Plasma cell Leukemia, a complication of Multiple Myeloma

Multiple Myeloma (Plasma Cell Myeloma)

Multiple Myeloma is a cancer of Plasma cells. Plasma cells are white blood cells that secrete large volumes of antibodies. Plasma cells originate in the bone marrow and are transported by the blood plasma and the lymphatic system. There is abnormal plasma cell production and a subsequent overabundance of monoclonal M protein which causes kidney problems and thickening of blood, also cause formation of mass in the bone marrow or soft tissue. When only one mass is present, it is referred as Plasmacytoma. When more than one mass is present, it is referred as Multiple Myeloma. Multiple Myeloma usually occurs in elderly and is more common in men.

Cause:

Ø  Unknown

Ø  Drinking alcohol and obesity are risk factors. Each increase of body mass index by 5 is supposed to increase the risk by 11%.

Ø  Familial predisposition to myeloma exists.

Survival:

Ø  Without treatment, survival is supposed to be around 7 months.

Ø  With current treatments, survival is usually 4 to 5 years.

Ø  Above mentioned survival periods are shocking for a newly diagnosed MM person but I would like to share my personal experience of the reality I believe the reason of such short life expectancy in my next note "Life Expectancy of Newly diagnosed Multiple Myeloma patient: My family's experience"

Symptoms:

1.      Bone pain: The diagnosis is incidental in 30% of cases, discovered during routine blood screening done for unrelated problems. 70% of patients have bone pain at presentation. Sudden pain, usually worse with movement and at night due to a broken bone in the spine, ribs, or elsewhere. Local bone damage and osteoporosis (general thinning of the bone)

2.      Anemia: Persistent tiredness and fatigue due to anemia. Anemia is because normal red blood cells are crowd by myeloma plasma cells.

3.      Kidney damage or failure: High Blood calcium level result in kidney damage, causing weight loss, nausea, thirst, muscle weakness, and mental confusion.

4.      Recurrent unexplained infections: Like pneumonia, sinus, or urinary infection

5.      Swelling over body, shortness of breath or evidence of heart or kidney failure.

6.      Bleeding: Bleeding resulting from thrombocytopenia. Bleeding from nose (Epistaxis) may be a presenting symptom.

 Lab test findings:

1.      Decrease Hb%, WBCs, Platelets

2.      Increased Bl. Calcium, Bl. Creatinine, Protein level in the blood and/or urine. A 24-hour urine collection for quantification of the Bence Jones protein (ie, lambda light chains), protein, and creatinine clearance is required.

3.      M-SPIKE: Presence of monoclonal protein in the blood and/or urine. The M-SPIKE is produced by the cancerous myeloma cells present in the bone marrow. In general, the amount of M-SPIKE reflects the amount of myeloma.

4.      Lytic bone lesions or osteoporosis. A conventional complete plain skeletal survey usually depicts lytic lesions.

5.      C-reactive protein (CRP) is useful for prognosis.

6.      Bone marrow aspirate and biopsy: To calculate the % of plasma cells,

7.      The Kappa/Lambda Ratio:

a.      When the level of either kappa or lambda is very high and the other chain is normal or low, then the ratio is abnormal and indicates that the myeloma is active.

b.      When the levels of both kappa and lambda light chains are increased, the ratio may be within the normal range, it generally indicates a disease other than myeloma, such as poor kidney function.

c.       When the kappa and lambda levels are both within the normal range but the ratio abnormal, then there may be a persistent low level of active myeloma with excess production of the abnormal light chains.

d.      A normal kappa/lambda ratio after treatment is a particularly good remission and is termed a stringent complete response. Normalization of the kappa/lambda ratio correlates with possible longer remissions.

 MGUS- monoclonal gammopathy of undetermined significance: This is predominantly a benign condition. The risk of developing active myeloma is very low: 1%/year. Thus, after 20 years, 80% of patients have not developed active myeloma. MGUS Diagnostic Criteria: All Three Required:

Ø  Serum monoclonal protein and/or urine monoclonal protein level low.

Ø  Monoclonal bone marrow plasma cells < 10%. Normal Serum Calcium, Hemoglobin and Serum Creatinine level.

Ø  No bone lesions on full skeletal X-ray survey and/or other imaging if performed.

Smoldering myeloma (low risk): Very similar to MGUS. Approximately 50% of patients will develop myeloma within 18-24 months. Smoldering or Indolent Myeloma Diagnostic Criteria: All Three Required:

Ø  Monoclonal protein present in the serum and/or urine

Ø  Monoclonal plasma cells present in the bone marrow and/or a tissue biopsy.

Ø  Not meeting criteria for MGUS, multiple myeloma, or solitary plasmacytoma of bone or soft tissue.

Plasma Cell Leukemia: A dreaded complication of Multiple Myeloma. The survival rate of these patients with present available treatment modalities are very poor.

Treatment:

1.      Currently No Cure for MM.

2.      Autologous stem cell transplantation, radiation and surgical care in certain cases, have helped to lessen the occurrence and severity of adverse effects of this disease.

3.      Chemotherapy and immunosuppression: Several drug therapies are valuable in the treatment of symptomatic MM.

a.      Thalidomide, either as a single agent or in combination with steroids.

b.      Lenalidomide plus dexamethasone

c.       Bortezomib plus melphalan

d.      VAD (vincristine, doxorubicin and dexamethasone)

e.      Melphalan plus prednisone

4.      Adjunctive therapy may also include:

a.      Erythropoietin

b.      Surgical intervention

c.       Plasmapheresis

5.      Autologous Stem Cell Transplant: The first step before starting therapy in MM is to determine whether a patient is a candidate for an autologous stem cell transplant. Eligibility depends primarily on the patient’s age and comorbidities. Typically an age of 65 years is used as a cut-off point for transplant eligibility. Using the patient’s own bone marrow or peripheral blood stem cells facilitates more intense therapy for MM. After harvesting the stem cells from the patient, physicians can use otherwise lethal doses of total body irradiation and chemotherapy and then “rescue” the patient by reinfusing the harvested cells.

6.      Physical Activity: Patients should be encouraged to be physically active to the extent appropriate for their individual bone status. Physical activity may help maintain bone strength.

7.      Black Cumin seed oil: Thymoquinone, an extract of black cumin seed oil is shown to be effective suppressor of tumour cell survival, proliferation and angiogenesis in patient of Multiple Myeloma in one study.

Warning: The purpose of this article is to create awareness for the disease mentioned above. The reader of this article should exercise all precautions before following any information provided above and it is advised that you consult your own physician or other medical professional. The responsibility lies solely with the reader and not with the site or the writer.