Tirthankar Online: January 2009

January 02, 2009

DIAGNOSIS OF SEPTICEMIA

Causative organisms:

(Mention those bacteria that you are well-conversant with)

Gram negative cocci – meningococci, gonococci, hemophilus
Gram negative bacilli – Salmonella typhi, EIEC, almost all causes of UTI, Infective endocarditis (including HACEK organisms), meningitis.
Gram positive organisms (rare) – Streptococcus, Staphylococcus, Pneumococcus, almost all organisms that cause osteomyelitis and pneumonia.

Material for diagnosis:

Venous blood – 3 samples at 0, 30 and 90 min intervals from admission
Urine
CSF (if features of meningeal irritation are present)
Swab from suspected skin lesion

Steps of diagnosis:
Exams and Tests

Physical examination may show:

Low blood pressure
Low body temperature or fever
Signs of associated disease (such as meningitis, epiglottitis, pneumonia, or cellulitis)

Tests that can confirm infection include:
Blood culture
Urine culture
CSF culture
Culture of any suspect skin lesion
CBC
Platelet count
Clotting studies
PT
PTT
Fibrinogen levels
Blood gases

BLOOD CULTURE
A minimum of 10 ml of blood is taken through venipuncture and injected into two or more "blood bottles" with specific media for aerobic and anaerobic organisms.
Care needs to be taken that the bottles are not contaminated with bacteria from staff members or other patients. To that end, the patient's skin is rubbed or sprayed with denaturated alcohol and betadine applied to the sampling site. Sterile gloves should be used to minimize contamination.
To maximise the diagnostic yield of blood cultures multiple sets of cultures (each set consisting of aerobic & anaerobic vials filled with 3-10 mL) may be ordered by medical staff.
Set 1= L. antecubital fossa at 0 minutes
Set 2= R. antecubital fossa at 30 minutes
Set 3= L. or R. antecubital fossa at 90 minutes
Ordering multiple sets of cultures increases the probability of discovering a pathogenic organism in the blood and reduces the probability of having a positive culture due to skin contaminants.
After inoculating the culture vials on the hospital floor, they are sent to the microbiology lab clinical pathology department. Here the cultures are entered into a blood culture machine, which keeps the samples at body temperature. The blood culture instrument reports positive blood cultures (cultures with bacteria present, thus indicating the patient is "septic") by monitoring carbon dioxide levels produced by bacteria in the vials via fluorescence detected by a light emitting diode (LED). Most cultures are monitored for 5-days, after which, if the vials are negative, they are removed.
If a vial is positive, a microbiologist will perform a Gram Stain on the blood for a rapid, general ID of the bacteria, which they will report to the attending physician of the septic patient. The blood is also subcultured or "Subed" onto agar plates to isolate the pathogenic organism for culture and suceptability testing, which takes up to 3 days time. This culture & sensitivity (C&S) process IDs the species of bacteria. Antibiotic sensitivities are then assessed on the isolate to inform clinicians on appropriate antibiotics for treatment.
Some guidelines for infective endocarditis recommend taking up to 6 sets of blood for culture (around 60 ml).

URINE EXAMINATION:
(Summarize the Laboratory diagnosis for UTI)
CSF EXAMINATION:
(Summarize the Laboratory diagnosis of Meningitis)

ROUTINE EXAMINATIONS
CBC - may show neutrophilia (enteric fever may show neutropenia)
Platelet count - may decrease following DIC
Clotting studies
PT - may rise following DIC r hepatocellular failure
PTT - may rise in DIC
Fibrinogen levels – may be low in DIC
FDP – may rise in DIC
Blood gases – may be abnormal in respiratory failure (raised pCO2 and low pO2)

CONCLUSION:
Based on the above investigations we can reach a diagnosis of septicemia.

Answers to your questions

2. Short note on SSSS.(Deborshi)

Ans:
Definition:

Staphylococcal scalded skin syndrome (SSSS) is an acute epidermolysis caused by a staphylococcal toxin.

Newborns and children are most susceptible. Symptoms are widespread bullae with epidermal sloughing. Diagnosis is by examination and sometimes biopsy. Treatment is antistaphylococcal antibiotics and local care. Prognosis is excellent with timely treatment.

Staphylococcal scalded skin syndrome (SSSS) almost always affects children < 6 yr (especially infants); it rarely occurs in older patients unless they have renal failure or are immunocompromised. Epidemics may occur in nurseries, presumably transmitted by the hands of personnel in contact with an infected infant or who are nasal carriers of Staphylococcus aureus. Sporadic cases also occur.
SSSS is caused by group II coagulase-positive staphylococci, usually phage type 71, which elaborate exfoliatin (also called epidermolysin), a toxin that splits the upper part of the epidermis just beneath the granular cell layer. The primary infection often begins during the first few days of life in the umbilical stump or diaper area; in older children, the face is the typical site. Toxin produced in these areas enters the circulation and affects the entire skin.

Symptoms and Signs

The initial lesion is usually superficial and crusted. Within 24 h, the surrounding skin becomes painful and scarlet, changes that quickly spread to other areas. The skin may be exquisitely tender and have a wrinkled tissue paper–like consistency. Large, flaccid blisters arise on the erythematous skin and quickly break to produce erosions. Intact blisters extend laterally with gentle pressure (Nikolsky's sign). The epidermis may peel easily, often in large sheets. Widespread desquamation occurs within 36 to 72 h, and patients become very ill with systemic manifestations (eg, malaise, chills, fever). Desquamated areas appear scalded. Loss of the protective skin barrier can lead to sepsis and to fluid and electrolyte imbalance.

Diagnosis

· Biopsy
· Cultures may be useful in adults

Diagnosis is suspected clinically, but confirmation usually requires biopsy (frozen section may give earlier results). Specimens show noninflammatory superficial splitting of the epidermis. In children, skin cultures are seldom positive; in adults, they are frequently positive. Cultures should be taken from the nose, conjunctiva, throat, and nasopharynx.

Differential diagnosis:

Differential diagnosis includes drug hypersensitivity, viral exanthemas, scarlet fever, thermal burns, genetic bullous diseases (eg, some types of epidermolysis bullosa), acquired bullous diseases (eg, pemphigus vulgaris, bullous pemphigoid), and toxic epidermal necrolysis. Stevens-Johnson syndrome is characterized by mucosal involvement, which is absent in SSSS.

Differentiating Staphylococcal Scalded Skin Syndrome (SSSS) and Toxic Epidermal Necrolysis (TEN)

SSSS

i)Patients affected - Infants, young children, immunocompromised adults

ii)Patient history - Recent staphylococcal infection, renal failure

iii) Level of epidermal cleavage (blister formation)* - Within the granular cell (outermost) layer of the epidermis

TEN

i)Patients affected - Older patients

ii)Patient history - Drug use

iii)Level of epidermal cleavage (blister formation)* - Between the epidermis and dermis or at the level of the basal cell

*Determined by Tzanck test or by a frozen section of a fresh specimen.

Treatment

· Antibiotics
· Corticosteroids not recommended
· Gel dressings for weeping lesions

With prompt diagnosis and therapy, death rarely occurs; the stratum corneum is quickly replaced, and healing usually occurs within 5 to 7 days after start of treatment.Penicillinase-resistant antistaphylococcal antibiotics given IV must be started immediately.

1. Comment: carcinoma usually spreads through lymphatics. (Himel)

Answer: It is a common dictum that carcinomas usually spread via lymphatics, and sarcomas usually spread through blood vessels. Most carcinomas metastasise by lymphatics, which include Ca breast, Ca stomach, Ca uterus, etc. However, it is not a universal dictum, as some Ca preferencially spreads via blood vessels, like renal cell carcinoma.

Recent research has thrown light on the probable reason behind this peculiar preference. The tumors that spread via blood vessels produce sufficient local angiogenesis, so that the tumor is well supplied by micro vessels that help in hematogenous spread. However, tumors that metastasise through lymphatics are rarely supplied with micro lymphatics. Instead, they have a surrounding chain of lymphatics outside the tumor mass. The spread into these vessels is facilitated if the surface area of the micro lymphatics can be increased or if the growth of intra-tumor lymphatics can be facilitated.. It is seen that the carcinomas that spread via lymphatics secrete higher amounts of VEGF-C, VEGF-D, VEGF-A and PDGF-BB, the growth factors that increase the number and the surface area of the lymphatics and facilitates the invasion by tumor cells. The higher expression of VEGF gene in carcinomas compared to sarcomas may explain why carcinomas more often spread via lymphatics.