Page 591 - ACCCN's Critical Care Nursing

568 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

subendothelial surface, activation of factors XI, XII, X, such as in purpura fulminans or ischaemia in the extremi-
8
VIII, calcium and phospholipid. The final pathway is ties. 47,48 Administration of APC in its role as inhibitor of
production of thrombin which converts soluble fibrino- the coagulation cascade is controversial. A Cochrane
gen to fibrin. Fibrin and aggregated platelets form intra- review of four studies involving 4911 participants (4434
vascular clots. adults and 477 paediatric patients) identified no reduc-
tion in risk of death (28-day mortality) in adult partici-
Inflammatory cytokines also initiate coagulation though
activation of tissue factor (TF), a principal activator of pants with severe sepsis, but was associated with a higher
coagulation. Endotoxins increase the activity of inhibi- risk of bleeding. Effectiveness was not associated with the
49
tors of clot breakdown (fibrinolysis). Levels of protein C degree of severity of sepsis. Studies continue into this
and endogenous activated protein C are decreased in area of clinical practice.
sepsis; this inhibits coagulation cofactors Va and VIIa and
acts as an antithrombotic in the microvasculature. 8 Endocrine Dysfunctions
Numerous endocrine derangements are noted in critically
Microvascular thrombosis that leads to MODS results ill patients, including abnormalities in thyroid, adreno-
from two major syndromes: thrombotic microangiopathy cortical, pancreas, growth and sex hormones. A high thy-
(TMA) and disseminated intravascular coagulation (DIC). rotropin (TSH) level is a significant independent predictor
TMA is characterised by formation of microvascular plate- of non-survival in critically ill patients, while subclinical
50
let aggregates and occasionally fibrin formation. Typically hypothyroidism has significant negative effects on cardiac
there is history of injury to the microvascular endothe- function and haemodynamic instability. 50,58
lium (e.g. thrombotic thrombocytopenic purpura, hae-
molytic uremic syndrome, haemolytic anaemia, elevated Adrenal Insufficiency
liver enzymes and low platelet syndromes of pregnancy
44
or antiphospholipid antibody syndrome). TMA usually Adrenal insufficiency is present in approximately 30% of
32,43,51,52
presents with normal coagulation profiles such as pro- patients with sepsis or septic shock, and is associ-
thrombin times and partial thromboplastin time. 44 ated with chronic adrenal insufficiency and recent physio-
50
logical stress, or in new-onset adrenal insufficiency. This
Disseminated intravascular coagulation results from adrenal insufficiency can be caused by sepsis, surgery,
widespread activation of tissue factor-dependent coagula- bleeding and head trauma. Adrenal insufficiency as a
tion, insufficient control of coagulation and plasminogen- cause of shock should be considered in any patient with
mediated attenuation of fibrinolysis. This leads to hypotension with no signs of infection, cardiovascular
44
formation of fibrin clots, consumption of platelets and disease or hypovolaemia. Incidence ranges from 0–95%,
53
coagulation proteins, occlusion of the microvasculature, partly because there is no standard definition for adrenal
and resultant reductions in cellular tissue oxygen deliv- insufficiency.
44
ery. DIC is most commonly a result of trauma or sepsis
and is an exaggerated response to normal coagulation Eosinophilia (>3% of total white blood count) is reported
aimed at limiting infection, exsanguination and promot- as a marker of adrenal insufficiency. Methods to diagnose
ing wound healing. 44 acute adrenal insufficiency include: (1) a single random
cortisol level check, or a change in cortisol level after
3
Thrombocytopenia (a platelet count of <80,000/mm or endogenous adrenocorticotrophic hormone (ACTH) is
a decrease of ≥50% over the preceding three days) signi- administered; or (2) a short corticotrophin stimulation
45
fies haematological failure, with leucocytopenia/cytosis, test with administration of high-dose ACTH. A change in
46
markers of coagulation and DIC also present. Treatment cortisol level (≤9 µg/dL) is considered relative adrenal
is supportive and aimed at removing the triggering insults. insufficiency. It is however argued that patients with
Clinical biomarkers include a simultaneous rise in pro- severe sepsis may have appropriate cortisol levels, but not
34
thrombin time, APTT and thrombocytopenia. A patient the reserve function to respond to the stimulation test. 31
may exhibit bleeding from puncture sites (e.g. invasive
vascular access), mucous membranes including bowel, or Steroid Therapy
upper gastrointestinal tract. Bruising or other subcutane- As septic shock is a major complication of infectious
ous petechiae may be evident. The skin should be pro- processes, the relationship between the immune, coagu-
tected from trauma. 54
lation and neuroendocrine systems has been explored.
Primary therapy is directed at the cause of the insult, with The role of corticosteroids in the treatment of septic
SIRS, ischaemia, uraemia, hepatotoxins and sources shock has led to a number of trials that suggested some
of infection, injury or necrosis managed concurrently. survival benefit for low-dose corticosteroid therapy. More
Aggressive resuscitation includes crystalloid or colloid research is required, however, because of conflicting find-
administration, replacement of blood components and ings from individual studies.
clotting factors using packed cells, platelets, cryoprecipi- Therapy with corticosteroids at a physiological dose,
tate and fresh frozen plasma. Endpoints for haemoglo- rather than a high dose, followed observations that
bin, platelets and coagulation levels have not been agreed patients with septic shock who had a reduced response
upon and replacement is therefore individualised. 47
to corticotropin were more likely to have increased mor-
The role of heparin or fractionated heparin is controver- tality, and that pressor response to noradrenaline may be
55
sial in the presence of sepsis, particularly in those with improved by the administration of hydrocortisone. A
overt thromboembolism or extensive fibrin deposition, trial exploring steroid use in sepsis demonstrated reduced