Showing posts with label Health. Show all posts
Showing posts with label Health. Show all posts

Wednesday, November 25, 2015

Sepsis

SEPSIS
By Dr. LORN SAKANA
Emergency department Stung Treng Referral Hospital

Objective:
  1. Definition
  2. Classification or degree of sepsis
  3. Etiology
  4. Diagnosis
  5. Management
  6. Monitoring
Definition:
Systemic Inflammatory Response Syndrom (SIRS):
SIRS criteria: two or more of:
•Temperature more than 38 C or  less than 36 C
•Heart Rate more than 90/min
•Respiratory rate more than 20/min
•WBC > 12,000/mm3 - 4,000/mm3

Not including any other type of inflammation like burn, trauma, SLE, Thyroid storm…

Classification of degree of sepsis:

  1. Sepsis
  2. Severe sepsis
  3. Septic shock
1. Sepsis: Presence of SIRS criteria due a culture or biology proven infection or an infection identify by clinical examination.

2. Severe sepsis: 
                          Sepsis + one of the following signs of:
  • Area of mottled skin
  • Capillary refill > 3seconds
  • Urine output less than 0 -.5-1ml per hour
  • Mental status change brutally
  • Platelet < 100,000/ml
  • Disseminated intravascular coagulation
  • Acute respiratory distress syndrom (ARDS)
3. Septic shock:

Sepsis + Hypotension
•Hypotension:
Main Artery Pressor(MAP) less than 60mmHg
Main Artery Pressor(MAP) less than 80mmHg (HTN patient)
Etiology:

Risk factors:
  • Compromised immune system: HIV, Cancer, Diabetic...
  • Very old and young patient
  • Uncompleted antibiotherapy
  • Associated with many health problem...
Develop from other infection:
  • Respiratory focus
  • Abdominal source
  • Urinary focus
  • Septic arthritis
  • Bacteria meningitis
  • Skin and soft tissue infection
The most frequent etiological argent:
  • Staphylococcus aureus (Rarely non aureus staphylococci)
  • Streptococci (Pneumococcus and other)
  • E-Coli and other Enterobacteriacease (Klebsiella sp, Enterobacter sp.)
  • Salmonella Typhi/Paratyphi A and non-typhoid Samonella
  • Burkhoderia pseudomallei (Melioidosis)
Diagnosis:

Clinical argument:
  • Predisposing condition: Underlying disease that cause immune deficiency (Diabetic, HIV, steroid use, liver cirrhosis, chronic renal disease, cancer, chemotherapy...)
  • Clinical syndroms/sign: Present of SIRS criteria's plus other soft infection:
    • Respiratory focus: tachypnea (RR>25/min), signs of consolidation (decrease Breathing sound/vocal vibration, crackle, localized dullness...) 
    • Urinary tract infection (UTI): dysuria, urinary frequency and urgency, abdominal pain, altered mental status...
    • Septic arthritis: A warm, swollen and painful join(s) with restricted movements...
    • Bacteria meningitis: Classic triad (Fever, headache, neck stiffness), Bruzenski's sign, Kernig's sign...
    • Skin and soft tissue infection: Skin lesion, cutaneous hemorrhage, blister with dark fluid...
Investigation:

  • CBC, Creatinine, Urea, electrolytes, transaminase, blood sugar.
  • Blood culture
  • Urine analysis, urine microscopic, urine culture
  • CSF examination or CSF culture
  • Pus culture
  • Malaria smear
  • Serum amylase (if suspect pancreatitis)
  • HIV Test
  • Chest X-Ray
  • Abdominal ultrasound
Management:
  1. Stabilize the patient:
  • Stabilize the patient according to ABC (Air ways, Breathing, Circulation)
  • IV Fluid resuscitation: NSS or Ringer Lactat
    • 20 - 60ml/kg for the first 6 hours (Max 4 - 6L over 24h
    • Dopamine 5micrograme/kg/min (max 20 micrograme/kg/min) if IV fluid challenge is unsuccessful at least 3 - 4L in the first 1 - 2h
  • If have signs of Disseminate Intravascular Coagulation (DIC) or hypoxia should be  transfusion even Hemoglobin > 7g/dl
    • The goal of fluid resuscitation:
      • Improve vital signs
      • Urine output > 0.5 - 1ml/h
   2.  Treatment causal:
  • Sepsis from respiratory focus:
    • 1st line: Amoxicilline - clavulanic acide: 1000/250mg    q4-6h (IV)
    • 2nd line: Ceftriaxone: 2g   qD (IV)
      • If severe sepsis with ARDS: add Gentamicine: 1-2.5mg/kg/dose q8h - q12h (IM/IV)
  • Sepsis from abdominal source:
    • 1st line: Ceftriaxone: 2g   qD   (IV)
    • 2nd line: Amoxicilline - clavulanic acide: 1000/250mg   q4-6h (IV)
      • If severe sepsis or septic shock: add Gentamicine: 1-2.5mg/kg/dose q8-12h (IM/IV)
  • Sepsis from urinary focus:
    • 1st line: Ceftriaxone: 2g  qD  (IV)
      • If severe sepsis or septic shock: add Gentamicine: 1-2.5mg/kg/dose q8-12h (If renal function work well)
  • Septic arthritis:
    • 1st line: 
      • Cloxacilline: 2g q4H (IV) + Ampicilline: 2g q4h or Penicilline 4MIG q4h (IV) + Gentamicine loading dose 3mg/kg IV then 1mg/kg q8h
  • Sepsis by bacteria meningitis:
    • 1st line: Ceftriaxone: 2g q12h (IV)
      if very young or very old and immune deficiency patient: add Ampicilline: 2g q4h (IV)
    • Dexamethazone: 8-10mg q8h IV for 5 days
  • Skin and soft tissue infection:
    • Cloxacilline: 2g q6h (IV)
    • In case Penicilline allergy: Limcomicine 600mg q8h (IV)
    • If suspect melioidosis:
      Ceftriaxone: 2g q8h (IV)
      Cotrimaxazole 8/40mg/kg q12h (PO) Plus Folic acide 5mg qD (PO)
Monitoring:

•Clinical monitoring:
–Urine output
–Vital signs, Consciousness level
–Blood sugar: if BS > 150mg/dl (finger stick)
•Laboratory monitoring:
–BS (Goal < 150mg/dl)
–Ht > 21%
–CBC, creatinine…

  

Thanks


Tuesday, November 24, 2015

Cardic beriberi or Shoshin beriberi

CARDIAC BERIBERI OR SHOSHIN BERIBERI


I.      DEFINITION :
Infant Beriberi, a disease caused by the mother's thiamine deficiency. The heart of infant is primarily affected and these infants have classical heart failure and sudden death.

II.      ETIOLOGY
·    Beriberi can occur in breast-fed infants when the mothers body is lacking in thiamine.
The condition can also affect infants who are fed anusual formulas that don’t have enough
thiamine.
·    Beriberi may be found in mother whose diet consists mainly of polished white rice, which is very low in thiamine because the thiamin-bearing husk has been removed.
·    It can also be seen in mother chronic alcoholics, arsenic poisoning
·    A rare condition known as genetic beriberi is passed down through families. People with genetic beriberi lose the ability to absorb thiamine from foods
·    The peak prevalence of this form occurs in fat breastfed babies of 2-12 months with predominant pick of 3 months of age.(14)

III.      PATHOPHYSIOLOGY


·    Thiamin acts as coenzyme to produce acetylcholine, a neurotransmitter(messenger between nerve fibers) :
o It is needed as TTP for nerve and muscle function..TTP (thiamin triphosphate )
activates ion channels in nerve and muscle cells by phosphorylating them.
The flow of the electrolytes, such as sodium and potassium in and out of the cell plays a role in nerve impulse conduction and voluntary muscle action
o It is essential as TPP for metabolism of carbohydrates into simple sugars, such as glucose. Thiamin Pyrophosphate is a coenzyme for pyruvate dehydrogenase complex and alpha-ketogluterate dehyrgoenase complex which is required in the Citric Acid Cycle(Kreb cycle ) to extract energy from food . In this process TPP acts as a dehydrogenase and removes CO2 .
o Phosphorylation- the process of transferring a phosphate group,from one molecule to  another. In this illustration the phosphate is being taken from the Adenosine
Triphophate and placed on the protein leaving Adenosine Diphosphate .
·    Deficiency of thiamine affects the cardiovascular, muscular, nervous, and GI systems :
o Cardiomegaly and congestive heart failure, with a characteristic high cardiac
output presumablyrelated to low peripheral resistance, is seen in thiamin deficiency
and is termed cardiac (Shoshin) beriberi.
o Lactate acidosis : due to pyruvate dehydrogenase complexactivity decreased, acetic acid and pyruvic acid  increase . the accumulation of lactic acid in the brain, may lead to impairment of respiratory and kidney function.
o Gastrointestinal System: Thiamin deficiency can also lead to nausea,lack of appetite, weight loss and constipation . Carbohydrate digestion and the metabolism of glucose are diminished.
o Neurologic Problems : reduces  absorption ,alters metabolism and depletes body stores. mental confusion, visualdisturbances , staggering gait, depression, irritability and reduced ability to concentrate are later followed by fatigue, muscle cramps and various pains.

IV.      CLINICAL ASSESSMENT
1.   High risk mother:
·    Low socio-economic status
·    Peripheral oedema and tender sole
·    Intermittent paraesthesiae in the hands and feet during and after pregnancy without subjective or clinical evidence of neurological deficit.
·    Excessive alcohol intake
2.   Infant present history
·    Breast feeding from high risk mother
·    Sibling died with the same symptoms
3.   Urgent clinical signs and symptoms
·    Acute respiratory distress and characteristic horse voice (Aphonic beriberi)14
·    Lethargy or drowsiness14
·    Shortness of breath (clear lung) with or without shock7
·    Central and peripheral cyanosis10, 11, 12
·    Liver enlarged and low urine output14,7
·    Convulsion14
·    Poor feeding10, 11, 12,13
4.   Imaging Studies
·    Chest radiography: cardiomegaly (mean cardiothoracic ratio 56,1%)
·    Heart ultrasound14:
o Cardiomegaly (right ventricular hypertrophy and dilatation)
o Pulmonary arterial hypertension
o Tricuspid valve regurgitation
·    MRI descriptions in this condition. These infants had involvement of the frontal lobes and basal ganglia, in addition to the lesions present in the periaqueductal
region, thalami, and the mammillary bodies that have been described in adults. The lesions that have been noted were described as symmetric and hyperdense. Brainstem involvement was noted. In small numbers of patients severe frontal
damage was noted in long term follow-up with a loss of parenchyma and atrophy of the basal ganglia and thalami in some.
5.   Laboratory Study
·    Thrombocytosis ( Platelet count > 400000/mm3 80% of cases)14
·    Metabolic acidosis (62% of cases)14
·    Thiamin in blood or urine
·    Erythrocyte transketolase (ETK) activity test
·    Blood lactate & pyruvate

Note: The most rapid, and thus the best diagnostic test for beriberi in urgent situations, is observing a clinical response to administration of intravenous thiamine (few hours duration)
V.      MANAGEMENT: Assess ABCD:

A – Airway

·    Position the head - neutral position (<1 year old), or sniffing position  (1 year of age)
·    Open airway - Head tilt and chin lift, or jaw thrust
·    Use oro-pharyngeal airway if required.

B – Breathing
·    If respiration is adequate, administer oxygen by facemask at 10 l/min.
·    If the child is not breathing, commence artificial ventilation  ( See APLS)

·       Intubation should only be attempted by those credentialed and skilled to do
(see APLS)

C – Circulation

·    If there are no signs of circulation, i.e. no pulse, slow pulse (<60) or you are not sure, commence CPR (cardiopulmonary resuscitation), and determine the cardiac rhythm - display the ECG

D- Drugs to consider: Thiamine2

·    Day 1: Dilute 1 ml of thiamine (vial 1 ml - 100 mg) with 9 ml of water for injection. Inject 1 ml of this diluted solution (10-mg thiamine) by slow IV. Repeat after 30 minutes. Then, give 25 mg by IM to  complete the first day treatment.  If
IV access is not possible, give 50 mg/day by IM divided in 2 injections over the first 24 hours.
After thiamine administration ,the smaller dose sodium bicarbonate may also be prescribed for management of lactic acidosis13

·    Day 2: It is usually possible to switch to PO treatment:
o If the infant is breast-fed: treat the mother with thiamine PO 100 mg/day for 1 month.
o If the child has been weaned: treat the child: with thiamine PO 10 mg/day for 1 month.

VI.      PATIENT/PARENT EDUCATION:
Population at risk must be educated regarding:
·     The diversification of diet.
·     The incorporation of foods rich in thiamine (liver, brown rice, green leaves, and potatoes).
·    Proper food preparation (shorter cooking time for vegetables, reduction in amount of rice washing prior to cooking).
·    The value of whole grains.
·    Avoidance of alcohol.
·    Thiamine supplementation.



REFERENCES
1.   Clinical Practice Guidelines, Dept. of General Medicine, The royal children's hospital
Melbourne. Australia.
2.   Clinical Practice Guidelines, for referral hospital,Cambodge,1999
3.   Katsura E, Oiso T, Beiberi, WHO, Chapiter 9,136-145
4.   Simon S Rabinowitz, Batres, Sheela Moorthy, Beriberi,  eMedicine Specialties > Pediatrics: General Medicine > Nutrition, Sep 18, 2009
5.   Nicola J et al, Beriberi. The major cause mortality in Caren refusees, Transaction of the royal society of tropical medicine and hygiene (2003) 97, 2051-2055.
6.   Loma-Osorio P., Penafiel P., Doltra A., Sionis A., Bosch, Shoshin Beriberi Mimicking a High-risk Non-ST-Segment Elevation Acute Coronary Syndrome with Cardiogenic Shock: When the Arteries are Not Guilty, J Emerg Med. 2008 Oct 17.
7.   Raidoo DP et al, Clinical diagnosis of cardiac beriberi, SAMJ, Volum 77, 3 febr 1990.
8.   Greespon J,Samuel M Alaish, Shoshin Beriberi mimicking central line sepsis in a child with short bowel line syndrom,  world journal of pediatrics, volum6 N 04, november,2010
9.   AVIVA FATTAL-VALEVSKI, IRIS AZOURI-FATTAL, and al, Delayed language development due to infantile thiamine deficiency, developmental medicine and child neurology, original article, ª The Authors. Journal compilation ª Mac Keith Press 2008,DOI:
10.1111/j.1469-8749.2008.03161.x .
10. Christine Luxemburger 1'2'3 , Nicholas J. White 1'2'3 , Feiko ter Kuile l'e, H. M. Singh 4., Ir6ne Ailier-Frachon s,Mya Ohn 1, Tan Chongsuphajaisiddhi 2 and Francois Nosten, Beri- beri: the major cause of infant mortality in Karen refugees, TRANSACTIONS OF THE ROYAL SOCIETY OF TROPICAL MEDICINE AND HYGIENE (2003) 97, 251-255.
11. Douangdao Soukaloun1, Sue J. Lee2,3, Karen Chamberlain4, Ann M. Taylor2, Mayfong Mayxay1,2,5, Kongkham Sisouk1, Bandit Soumphonphakdy1, Khaysy Latsavong1, Kongsin Akkhavong1, DouangkhamPhommachanh1, Vanmaly Sengmeuang1, Khonsavanh Luangxay1, Theresa McDonagh6, Nicholas J, Erythrocyte Transketolase Activity, Markers of
Cardiac Dysfunction and the Diagnosis of Infantile Beriberi, PL0s neglected tropical diseases, February 2011 | Volume 5 | Issue 2 | e971.
12. D. P. NAIDOO, V. GATHIRAM, A. SADHABIRISS, F. HASSEN, Clinical diagnosis of cardiac beriberi, SAMJ VOL 77 3 FEB 1990.
13. D. P. NAIDOO, Beriberi heart disease in Durban, A retrospective study, SAMT VOL 72 15
AUG 1987.
14. Beriberi known as Kantha Bopha Syndrom (KB Sd), Kantha Bopha Children's Hospital, Cambodia