Infectious diseases in intensive care

Clinical picture

 * Three most important signs of bacterial meningitis:
 * 1) altered level of consciousness;
 * 2) fever;
 * 3) meningeal signs.

A characteristic sign is the onset development of a disorder of consciousness (within 24 hours). 90% of patients will develop somnolence, sopor or coma as a result of impaired consciousness. The condition is accompanied by severe sepsis and progresses fast to organ failure (distal organs are affected, i.e. distant from the site of infection).

Treatment in case of suspected bacterial meniningitis

 * 1) secure the airways;
 * 2) IV access;
 * 3) mechanical lung ventilation;
 * 4) anti-edematous treatment (diuretics, mannitol);
 * 5) immediate transport to the hospital (ICU);
 * 6) antibiotics administered only in the hospital, after blood cultures collection. Delayed ATB treatment does not worsen the prognosis of bacterial meningitis. An exception is in case of the meningococcal meningitis (invasive meningococcal disease), when third generation of cephalosporins is also administered during transport to the hospital (3 g of cefotaxime).

Diagnostics
In critically ill patients, lumbar puncture is performed while lying on one´s side. A minimum amount of cerebrospinal fluid is taken. Intracranial hypertension should be ruled out before removing fluid to minimize the risk of the occipital conus. Ophthalmological examination of the ocular background is used for quick orientation, where edema of the papilla of the optic nerve would indicate intracranial hypertension. Papillary edema indicates CNS status with a 24-hour delay. A CT scan of the brain is more accurate, but it often represents a long delay. Relative contraindications for lumbar puncture are focal brain process, papillary edema (or CT findings) and immunodeficient patients over 60 years of age (CT examination is preferred). Gram staining has a sensitivity of 80% in cerebrospinal fluid, a standard cultivation of 90% (cerebrospinal fluid, unlike blood, is a more favorable environment for bacteria because it does not contain immunoglobulins, which protect the CNS from autoimmune processes). PCR examination of cerebrospinal fluid is a backup examination, and is expensive. It is focused on the detection of bacterial (possibly viral) DNA.
 * Finding in cerebrospinal fluid in bacterial meningitis:
 * morphology: elevated leukocytes levels (leu > 1000/mm3), of which polymorphonuclear cells make up > 60&thinsp;%;
 * biochemistry: increase of lactate (> 3,5&thinsp;mmol/l), decreased glycocaemia, glucose coefficient (cerebrospinal fluid / blood)< 45&thinsp;% (standard: 50–60&thinsp;%), increased proteins (> 1,3&thinsp;g/l).

Pathophysiology
Loss of consciousness is caused by edema, which is cytotoxic (pneumococcus). The blood-brain barrier through which solutes enter the CNS is broken. This increases intracranial pressure, worsens perfusion and worsen hypoxia. Therefore, mild systemic hypertension is tolerated.

Treatment of cytotoxic edema

 * antiedematous drugs: mannitol, diuretics;
 * adjuvant therapy: controlled hypocapnia (causes vascular spasms), corticosteroids (stabilize membranes).

Sepsis
Sepsis is defined as SIRS (systemic inflammatory response syndrome). Bacteria may not be present in the blood (although it is in most of cases). Fungi, viruses, parasites, endotoxins or inflammatory agents can also cause sepsis. Sepsis is the leading cause of death in the ICU. This is related to higher morbidity of patients (aging population, invasive treatment or diagnostic procedures, immunosuppression,…). The most common etiological agents are bacteria, viruses in Africa causing hemorrhagic fevers, in Europe influenza viruses and in immunosuppressed cytomegalovirus.

Current definition of sepsis from 2015: Sepsis is a life-threatening organ dysfunction caused by dysregulated response to infection.

Criteria for the diagnosis of sepsis

 * 1) temperature > 38&thinsp;°C nebo < 36&thinsp;°C;
 * 2) heart rate > 90/min;
 * 3) respiratory rate > 20/min;
 * 4) paCO2 < 32 kPa;
 * 5) leukocytes > 12 × 109/l nebo > 10&thinsp;% rods.

Clinical severity of sepsis

 * 1) sepsis;
 * 2) severe sepsis (MOFS = multiorgan failure);
 * 3) septic shock – the most severe prognosis, circulatory failure occurs. Unlike other types (hypovolemic, cardiogenic, anaphylactic types of shock), during this phase of septic shock, the patient is pink, well-perfused, has warm limbs and has increased cardiac output. The arteriovenous shunts (A-V Shunts) are open, the blood goes to the internal organs, and deep organ hypoxia develops, which is caused by increased lactate.

Sepsis of nosocomial origin
Several factors contribute to nosocomial sepsis in ICU patients, such as intubation cannulas, urinary catheters, analgesia, which cause muscle relaxation and the accumulation of secretions, bedsores as a gateaway to infection, and poor general state with the production of the cortisol stress hormone and IL-10.

Most common types of nosocomial sepsis



 * 1) ventilator-associated pneumonia – intubation cannulas can be primarily infected, secondarily by the hands of hospital staff or endogenously by the penetration of gram-negative bacteria from the intestines. The cranial progression of bacteria is facilitated by reduced intestinal motility, increased pH in the stomach (administered by proton-pump inhibitors to prevent stress gastric ulcers) and gastroesophageal reflux. The limit for pneumonia to be considered as nosocomial is 48 hours. Earlier development is considered as community sepsis;
 * 2) catheter sepsis;
 * 3) urosepsis;
 * 4) bedsores.

Causative agents of nosocomial sepsis
The causative agents include almost exclusively gram-negative bacteria.
 * Pseudomonas aeruginosa (treatment: carbapenems, in case of colistin resistance);
 * Klebsiella;
 * Proteus mirabilis.

Polyradiculoneuritis
Polyradiculoneuritis is a post-infectious inflammatory process that affects peripheral nerves. There is a rapid development of sensory disturbances and motor impairment of the lower limbs. These disorders are symmetrical, motor disorders are also referred to as "glove-and-stocking" paresthesias.

Characteristics of polyradiculoneuritis

 * peripheral nerve impairment;
 * progression to ventilation failure;
 * typical association with certain pathogens: Campylobacter jejuni, Borrelia burgdorferi, Cytomegalovirus, HIV, Influenza Virus.

Diagnostics

 * lumbar puncture: discrepancy between cerebrospinal fluid cytology and proteinorachia. Proteins are elevated (> 1&thinsp;g/l) and pleocytosis is minimal.
 * MRI: without any signs of spinal compression;
 * serology: boreliosis, CMV, HIV.

Treatment and prognosis
The basics include monitoring the condition in order to detect possible ventilation failure and secure the airways and initiate mechanical lung ventilation. This is often accompanied by swallowing and micturition disorders, which should be noted. Hospitalization is necessary. In addition, high doses of immunoglobulins are administered, or plasmapheresis is performed. Immunoglobulins appear to be a safer alternative, they are preferred in children, plasmapheresis is just as effective, but cheaper method that was often described with a higher incidence of complications.

Complications
Serious complications of polyradiculoneuritis include:
 * progression of cranial nerve palsies;
 * respiratory failure;
 * persistence of residual paresis.