HYDROCORTISONE

In the critically ill patient, adreno cortical insufficiency should be considered when an inappropriate amount of inotropic support is required.
Baseline cortisol levels and short synacthen test do not predict response to steroid.
In patients who demonstrate a normal short synacthen test, but yet show a dramatic response to steroid, it is possible that the abnormality lies in altered receptor function or glucocorticoid resistance rather than abnormality of the adrenal axis. Baseline cortisol levels and short synacthen test are worthwhile to assess hypothalami c –pituitary–adrenal axis dysfunction versus steroid unresponsiveness.  Available as the sodium succinate or the phosphate ester

 Uses     

1. Adrenal insufficiency (primary or secondary)   
2. Prolonged resistant vasopressor dependent shock   
3. Severe bronchospasm    
4. Hypersensitivity reactions     
5. Fibroproliferative phase of ARDS (unlicensed)  Adjunct in  Pneumocystis carinii  pneumonia (see co-trimoxazole and pentamidine)      

Contraindications   
Systemic infection (unless specifi c anti-microbial therapy given)   
 Administration   
•   Adrenal insuffi  ciency   Major surgery or stress: IV 100–500 mg 6–8 hourly    Minor surgery: IV 50 mg 8–12 hourly    Reduce by 25% per day until normal oral steroids resumed or maintained on 20 mg in the morning and 10 mg in the evening IV     
•   Prolonged resistant vasopressor-dependent shock   Initial dose 50 mg IV bolus, 6 hourly for 5 days, then 50 mg 12 hourly for 3 days, then 50 mg daily for 3 days, then stop or 50 mg IV bolus followed by infusion of 10 mg/h for up to 48 hours     
•   Fibroproliferative phase of ARDS   IV infusion: 100–200 mg 6 hourly for up to 3 days, then dose reduced gradually     
• Adjunct in  Pneumocystis carinii  pneumonia (see co-trimoxazole and pentamidine)    IV: 100 mg 6 hourly for 5 days, then dose reduced to complete 21 days of treatment    The steroid should be started at the same time as the co-trimoxazole or pentamidine and should be withdrawn before the antibiotic treatment is complete   Reconstitute 100 mg powder with 2 ml WFI. Further dilute 200 mg and made up to 40 ml with sodium chloride 0.9% or glucose 5% (5 mg/ml)     
 How not to use hydrocortisone   
Do not stop abruptly (adrenocortical insuffi  ciency)   
 Adverse effects   
Perineal irritation may follow IV administration of the phosphate ester
 
Prolonged use may also lead to the following problems: 
•   increased susceptibility to infections 
•   impaired wound healing 
•   peptic ulceration 
•   muscle weakness (proximal myopathy) 
•   osteoporosis 
•   hyperglycaemia          Cautions     Diabetes mellitus 
Concurrent use of NSAID (increased risk of GI bleeding)     
Thanks   

8 elements of primary-health care (PHC)

Primary health care (PHC) is essential health care made universally accessible to individuals and acceptable to them, through full participation and at a cost the community and country can afford. It is an approach to health beyond the traditional health care system that focuses on health equity-producing social policy. Primary health-care (PHC) has basic essential elements and objectives that help to attain better health services for all.

There are 8 elements of primary-health care (PHC). That listed below-  

E– Education concerning prevailing health problems and the methods of identifying,  preventing             and controlling them.

L–  Locally endemic disease prevention and control.

E–  Expanded programE  of immunization against major infectious  diseases.

M– Maternal and child health care including family planning.

E–   Essential drugs arrangement.

N– Nutritional food supplement, an adequate supply of safe and basic nutrition.

T–   Treatment of communicable and non-communicable disease and promotion of mental health.

S–  Safe water and sanitation 

Incubation period of various communicable disease

Some disease and their incubation period

Shock(Critical care nursing )

Shock

■      Shock occurs when the circulatory system is no longer able to deliver enough 02 and vital nutrients to adequately meet the metabolic demands of the patient.

■       Although initially reversible,

■      prolonged hypo perfusion will eventually result in cellular hypoxia and the derangement of critical biochemical processes

■       From a clinical standpoint, shock can be divided into the following subtypes:

1.     Hypovolemic

2.     Cardiogenic 

3.     Obstructive

4.     Distributive

Hypovolemic

■      Hypovolemic shock results from an inadequate circulating blood volume owing to either profound dehydration or significant hemorrhage.

■      Traumatic hypovolemia is the most common type of shock encountered in patients <40 years of age

Cardiogenic

■      Cardiogenic shock occurs when the heart is unable to provide adequate forward blood flow secondary to impaired pump function or significant dysrhythmia.

■      Myocardial infarction is the leading cause of cardiogenic shock and typically occurs once -40% of the myocardium is dysfunctional.

Obstructive

■      Obstructive shock results from an extracardiac blockage of adequate venous return of blood to the heart

Example : -

q  Pericardial  Tamponade ,

q  Tension  pneumothorax

q  Massive  pulmonary  embolism [PE)).

Distributive

■      Distributive  shock occurs secondary to an uncontrolled loss of vascular tone

v       Example 

■      sepsis

■      anaphylaxis,

■      neurogenic shock

■      adrenal crisis

■       Neurogenic shock most commonly occurs in trauma patients with high cervical cord injuries and a secondary loss of sympathetic tone and should always be considered a diagnosis of exclusion.

■      Classically these patients will present with hypotension and a paradoxical bradycardia.

■      Suspect septic shock in elderly, immunocompromised, and debilitated patients who are toxic appearing despite only vague symptoms.

■      The prognosis for patients with cardiogenic and septic shock remains grave ,with mortality rates between 30% and 90%.

Pathophysiology  of shock

■      The pathophysiology of shock can be divided into 3 basic categories.

■      a systemic autonomic response

■      endorgan cellular hypoxia

■      The  secretion of proinflammatory mediators .

a systemic autonomic response

■      The autonomic system initially responds to widespread tissue hypoperfusion by globally increasing the overall cardiac output.

■      As tissue perfusion continues to decline,

■      the body shunts circulating blood away from less vital structures including the skin, muscles, kidneys, and splanchnic beds.

■      Reflexively, the kidneys activate the renin-angiotensin axis, prompting the release of various vasoactive substances, with the net effect to preserve perfusion to the most critical organs, namely the brain and the heart.

■       When the preceding response is inadequate despite maximal tissue 02 extraction, cellular hypoxia forces a conversion from aerobic to anaerobic metabolism.

■       By nature, anaerobic metabolism cannot produce enough adenosine triphosphate to maintain regular cellular function.

■       Tissue lactate accumulates, resulting in systemic acidosis, and eventually this breakdown in cellular metabolism leads to widespread tissue death.

■      Injured and dying cells prompt the production and secretion of harmful inflammatory mediators,

■      resulting in the development of the systemic inflammatory response syndrome,

■       defined by the presence of fever, tachycardia, tachypnea, and leukocytosis

S3........lub - dub DUB normal in children and adults age up to 35 to 40 yrs  abnormal....HF
S4......LUB lub - dub
Abnormal...vent. hypertrophy due to HTN CAD cardiomyopathy aortic stenosis
When both s3 and S4 occurs...LUB lub - dub DUB refers as summation gallop