Bimonthly internal assessment

 CASE 1:

55 year old male patient came with the complaints of 

Chest pain since 3 days

Abdominal distension since 3 days

Abdominal pain since 3 days and decreased urine output since 3days and not passed stools since 3days 

https://sreejaboga.blogspot.com/2020/11/is-online-e-log-book-to-discuss-our.html?m=1

1.Anatomical locations and etiological possibilities:

A.Pancreas:acute severe pancreatitis secondary to gall stones

B.Kidney:Acute kidney injury secondary to pancreatitis

C.lungs:Right pleural effusion secondary to acute severe pancreatitis

Pleuropulmonary abnormalities are commonly associated with pancreatitis, respiratory dysfunction is rarely seen at the time of presentation to Emergency department (ED) but usually develops after fluid resuscitation. It manifests as acute lung injury or acute respiratory distress syndrome. It is one of the major components of multiple organ system dysfunction syndromes. Other manifestations are bilateral infiltrates, pleural effusion, pulmonary hypertension, and decreased thoracic compliance 

https://www.intechopen.com/books/intensive-care/severe-acute-pancreatitis-and-its-management

D.Tibia:diaphyseal dysplasia

E.Right upper limb:atherosclerotic vascular disease

due to hypertriglyceridemia

During the first 1-2 wk, a pro-inflammatory response occurs, which results in systemic inflammatory response syndrome (SIRS), a sterile response in which sepsis or infection rarely occurs. If the SIRS is severe, then proinflammatory mediators can cause early multiple (respiratory, cardiovascular, renal, and hepatic) organ failure

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4194569/

Sequence of events

A.diaphyseal dysplasia of both tibia

B.patient is a alcoholic and smoker since 30years

C.patient has an atherosclerotic vascular disease of right upper limb

D.patient presented with chest pain,sob, decreased urine output(due to AKI secondary to sepsis),constipation(due to paralytic ileus),abdominal distension

He was diagnosed with acute severe pancreatitis(supported by clinical,USG findings and raised serum amylase levels) secondary to gall stones with AKI ,rt pleural effusion

E.patient was started on inj.lasix and iv antibiotics,after 1day pedal edema and sob decreased.after one moreday patient was in altered sensorium,on the same day patient was taken for hemodialysis 1st session.after hemodialysis his urea and creat values have come down(7.4 to 5.3)and sensorium improved.

 F.After 2days patient was taken for one more session of dialysis (his creat 5.9 to 4.4) but his total leukocyte counts have been raised ?Central line sepsis.

G.within 24hrs of 2nd session of dialysis his creat increased again to 5.4 and patient had 8episodes of vomitings and was intolerant to oral feeds.

NON PHARMACOLOGICAL interventions

1.NBM:

2.Ryles tube:If nutritional support is supplemented by the enteral route, then it is usually delivered by tube feeding. There is a controversy about nasogastric versus nasojejunal feeding. But there is not much evidence to support any one over the other. Though traditionally nasojejunal feedings (to be delivered distal to the ligament of Treitz) have been preferred with the concept of less stimulation of the exocrine pancreas, cholecystokinin (CCK) cells that are present in the distal third part of the duodenum get stimulated when food passing through duodenum. It releases CCK that stimulates the pancreas and increased volume of pancreatic enzymes and bicarbonate secretion. This may worsen the course of the disease. Nasogastric tube feedings have now been shown to as safe as the jejunal feeding. Nasogastric insertion can be at bedside. Fluoroscopy endoscopic (endoscopically placed guide wire) and specialist help is not needed. With the Nasogastric (NG) feeding, the standard precautions of aspiration like elevation of head end of bed should be followed.

https://www.intechopen.com/books/intensive-care/severe-acute-pancreatitis-and-its-management

3:Oxygen support:Patients with acute severe pancreatitis should be monitored closely for early detection of failure. Respiratory support usually initiated by supplemental oxygen and mechanical ventilation is often required depending on the severity of respiratory dysfunction. Nasogastric decompression will decrease the distension and improve the compliance and prevent aspiration. Non-invasive ventilation is poorly tolerated in most of the patients because of abdominal distension and reduced functional residual capacity, careful selection of patient is warranted. Non-invasive ventilation is good choice to start with as it may avoid endotracheal intubation. Acute lung injury and Acute respiratory distress syndrome (ARDS) secondary to acute severe pancreatitis is similar to any other condition using lung protective strategies. Pleural effusion may need ultrasound-guided drainage. Good analgesia will help in chest physiotherapy, early physiotherapy will prevent atelectasis and related complications 

PHARMACOLOGICAL interventions

1.Iv fluids:Hypotension is one of the most common presentations with acute pancreatitis. It is a sign of impending organ dysfunction. The hypotension is due to the third space loss secondary to the inflammatory response, this contributes to hypoperfusion and end organ perfusion dysfunction. Aggressive fluid resuscitation and rapid restoration of intravascular volume are the main stay of the treatment. It requires several liters of fluids. Both crystalloids and colloids can be used as resuscitation fluids

https://www.intechopen.com/books/intensive-care/severe-acute-pancreatitis-and-its-management

2.Diuretics:for decreased urine output and renal failure

3.Antibiotics:

Role of antibiotic prophylaxis in severe acute pancreatitis

Prophylactic antibiotics in severe acute pancreatitis have been a topic of debate in the last 4–5 decades. Pancreatic necrosis more than 30% increases the chances of infection. The right choice of antibiotics is very important, those which have high penetration into pancreatic tissue. Carbapenems are both broad spectrum and excellent pancreatic penetration properties. Other antibiotics, which penetrate well in the pancreatic tissue, are cephalosporin, ureidopenicillins, fluoroquinolones, metronidazole and imipenem. Aminoglycosides have a poor penetration ability. Patients with mild pancreatitis do not benefit from antibiotics. In a meta-analysis by Sharma et al. [16], use of prophylactic antibiotics has shown mortality benefit in patients with Acute necrotizing pancreatitis (ANP) confirmed by contrast-enhanced CT (21–12.3%). Ref. [15, 16] prophylactic antibiotics use has not shown to decrease the need for interventional and surgical management but no effect on mortality.

https://www.intechopen.com/books/intensive-care/severe-acute-pancreatitis-and-its-management

4.ANALGESIA:Pain is one of the symptoms of acute severe pancreatitis. It causes discomfort and heightened sympathetic activity, impairment of oxygenation due to restriction of abdominal wall movement. Effective analgesia can be provided by the use of opioids and parenteral route, i.e. intravenous route is the preferred route. Analgesia may improve pulmonary dysfunction. In the past, morphine was supposed to exacerbate acute pancreatitis by promoting contraction of the sphincter of Oddi and increase pressure in the sphincter of Oddi dysfunction, but there is no good supportive evidence. Another modality of pain management is use of drugs like local anaesthetics through in epidural route 

https//www.intechopen.com/books/intensive-care/severe-acute-pancreatitis-and-its-management

CASE : 2

2) A 55 year old male, shepherd by occupation, presented to the OPD with the chief complaints of fever (on and off), loss of appetite, headache, body pains, generalized weakness since 2 months, cough since 2 weeks and vomitings and pain abdomen since 2 days. 

https://aakansharaj.blogspot.com/2020/11/55-year-old-male-with-anemia.html?m=1

A) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes. 

ANATOMICAL LOCATIONS WITH ETIOLOGY:

BONE MARROW

Etiology: Multiple myeloma

KIDNEYS

Etiology: AKI due to multiple myeloma

HEMATOLOGICAL (ANEMIA)

Etiology: secondary to multiple myeloma

LUNGS

Etiology: Tuberculosis (Increased susceptibility to infections)

TIMELINE OF EVENTS:

Alcohol & smoking (35 years) 

!

Stopped alcohol (4 years)

!

Fever , generalised weakness & anemia - 2 units blood transfusion (1.5 years)

!

Stopped smoking (4 months)

!

Low grade fever , generalized weakness , headache , neck pain , loss of appetite , weight loss (2 months) 

!

Cough & SOB (2 weeks) 

!

Vomiting & pain abdomen (2 days)

OUTCOME:

Some symptomatic relief and referred to higher centre in need for oncologist

B) What are the pharmacological and non pharmacological interventions used in the management of this patient and what are the efficacy of each one of them? 

PHARMACOLOGIC :

1.ANTIBIOTICS : For underlying infection (Azithromycin for ?Atypical pneumonia)

2.ATT : For TB

3.SEVELAMER : For hyperphosphatemia

4.FEBUXOSTAT : For hyperuricemia

5.PRBC transfusion for anemia

Case 3:

http://nithishaavula.blogspot.com/2020/11/51-yr-old-male-with-hfref.html?m=1

1)pedal edema with abdominal distention with sob suggestive of right heart failure or renal failure

B)etilogy of rt heart failure

https://www.ncbi.nlm.nih.gov/books/NBK459381/

chronic conditions of pressure overload may lead to RVF. These include:

Primary pulmonary arterial hypertension (PAH) and secondary pulmonary hypertension (PH) as seen in chronic-obstructive pulmonary disease (COPD) or pulmonary fibrosis)

Congenital heart disease (pulmonic stenosis, right ventricular outflow tract obstruction, or a systemic RV).

The following conditions result in volume overload causing RVF:

Valvular insufficiency (tricuspid or pulmonic) 

Congenital heart disease with a shunt (atrial septal defect (ASD) or anomalous pulmonary venous return (APVR)).

Another important mechanism that leads to RVF is intrinsic RV myocardial disease. This includes:

RV ischemia or infarct

Infiltrative diseases such as amyloidosis or sarcoidosis

Arrhythmogenic right ventricular dysplasia (ARVD)

Cardiomyopathy

Microvascular disease.

Lastly, RVF may be caused by impaired filling which is seen in the following conditions:

Constrictive pericarditis

Tricuspid stenosis

Systemic vasodilatory shock

Cardiac tamponade

Superior vena cava syndrome

Hypovolemia. 

2 )Pharmacological interventions

https://heart.bmj.com/content/104/5/407(meta analysis with each class of drugs)

Preload reducers

Diuretics

Afterload reducers-ace inhibitors

Rate controlling agents-beta blockers

Antiepileptics for known case of epilepsy

Insulin for glycemic control in diabetes.

Non pharmacological interventions

Salt and fluid restriction

https://pubmed.ncbi.nlm.nih.gov/23787719/

Individualized salt and fluid restriction can improve signs and symptoms of CHF with no negative effects on thirst, appetite, or QoL in patients with moderate to severe CHF and previous signs of fluid retention

CASE : 4

4) 31 yr old man with B/L pedal edema with scrotal and penile swelling since 2 months

https://nairaditya97.blogspot.com/2020/11/31-yr-old-male-with-bl-pedal-edema-with.html?m=1

A) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes. 

ANATOMICAL LOCATIONS WITH ETIOLOGY:

HEART FAILURE (pedal edema , penile & scrotal swelling and SOB) :

Etiology: Alcohol causing wet beriberi

AXONAL SENSORY POLYNEUROPATHY:

Etiology: Alcohol

EVENTS TIME LINE:

Alcohol & khaini (3 years) 

!

Pins and needles (1 year) 

!

Palpitations (8 months) 

!

PND (3 months) 

!

Pedal edema and SOB (2 months)

CURRENT OUTCOME: 

Completly relieved of his symptoms as the wet beriberi resolved.

B) What are the pharmacological and non pharmacological interventions used in the management of this patient and what are the efficacy of each one of them? 

PHARMACOLOGIC :

1.LASIX : Mortality: 3 placebo-controlled trials (n=221) reported data; the OR was 0.25 (95% confidence interval, CI: 0.07, 0.84, P=0.03), representing an absolute risk reduction of 8% in mortality in patients treated with diuretics compared to placebo.

Worsening of heart failure: 4 placebo-controlled trials (n=448) and 4 active-controlled trials (n=177) reported data. The OR was 0.31 (95% CI: 0.15, 0.62, P=0.001) for the placebo-controlled trials and 0.34 (95% CI:0.10, 1.21, P=0.10) for the active-controlled trials.

https://www.ncbi.nlm.nih.gov/books/NBK69174/

2.THIAMINE : In the study by Schoenenberger and colleagues (n=9), patients who took thiamine had 3.30% (95% confidence interval [CI]: 0.63%, 5.97%) greater LVEF compared to those on placebo.

Likewise, Shimon et al reported that thiamine resulted in 2.20% greater LVEF than the placebo group (n=29), although the extra improvement was not significant (95% CI: −18.97, 23.37%).

In our meta analysis, thiamine supplementation resulted in a significantly improved net change in LVEF (3.28%, 95% CI: 0.64%, 5.93%) compared with placebo.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3865826/#:~:text=Compared%20with%20placebo%20(2%20trials,0.64%25%2C%205.93%25).

3.TELMISARTAN : For afterload reduction in heart failure

NON PHARMACOLOGIC :

1.SALT AND FLUID RESTRICTION :

https://pubmed.ncbi.nlm.nih.gov/23787719/

Individualized salt and fluid restriction can improve signs and symptoms of CHF with no negative effects on thirst, appetite, or QoL in patients with moderate to severe CHF and previous signs of fluid retention