Anemia has also been identified as an adverse prognostic factor
mild (10 g/dl—normal),
moderate (8–10 g/dl), severe (6.5–8 g/dl) and life threatening (<6.5 g/dl or unstable patient) anemia
anemia in cancer patients is often multifactorial.
Cancer itself can directly cause or exacerbate anemia either by suppressing hematopoiesis through bone marrow infiltration
or production of cytokines that lead to iron sequestration, or by reduced red blood cell production
in inflammatory anemia, iron deficiency should be defined by a low transferrin saturation
of <20%, ferritin levels of <100 ng/ml and a low reticulocyte hemoglobin concentration of <32 pg
anemia to thrombocytosis, as commonly
seen in cancer patients
TNF-α inhibits hemoglobin production
treatment
itself may be a major cause of anemia
Other cytokines, such as interleukin-6 (IL-6), IL-1 and interferon-γ, have also been shown to inhibit erythroid precursors
in vitro [9], albeit to a lesser extent
In inflammation, from whatever cause, IL-6 induces the liver to produce hepcidin. Hepcidin decreases iron absorption from
the bowel and blocks iron utilization in the bone marrow
Numerous in vitro studies have illustrated the central role of TNF-α in the pathogenesis of anemia
nephrotoxic effects of particular cytotoxic agents such as platinum salts can also lead to the persistence
of anemia through reduced Epo production by the kidney
Currently two options are at the disposal of the clinician for the treatment of anemia in cancer patients: transfusion of
packed red blood cells and the use of erythropoiesis-stimulating agents (ESAs)
The goal of the treatment is to relieve the
symptoms of anemia such as fatigue and dyspnea.
Transfusion of 1 unit of packed red blood cells has been estimated to result
in an increase in the hemoglobin level of 1 g/dl in a normal-sized adult
a higher mortality rate in patients receiving
ESA treatment
Recent concerns regarding the risk of thromboembolism in patients treated with ESA have been corroborated by the meta-analyses
conducted by Tonnelli and Bennett
Great review of anemia in Cancer:
1) blood loss
2) increased RBC loss
3) decreased RBC production
Cancer infiltration of marrow can reduce hematopoiesis. Inflammatory cytokines can reduce hematopoiesis. Inflammatory cytokines can block Fe absorption. Chemo and radiation can cause anemia--particularily platinum based therapies.
delayed hemolytic events occur in ≈20% of patients with severe imported malaria, and 60% of these patients require blood transfusion
Delayed-onset anemia (herein referred to as postartesunate delayed-onset hemolysis [PADH] pattern of anemia) has been observed to occur 2–3 weeks after initiation of IV artesunate
The mechanism of this anemia is hemolytic, as demonstrated by high serum lactate dehydrogenase (LDH) and low plasma haptoglobin levels
PADH occurred in 27% of patients in this study, but it was rarely associated with severe anemia and was never fatal
median delayed drop in hemoglobin levels was 1.3 g/dL
This transfusion rate (<5%) is markedly lower than that previously reported for patients with severe imported malaria and delayed-onset anemia (≈60%)
Side effects of artesunate frequently include gastrointestinal disturbances, neutropenia (1.3%), reticulocytopenia (0.6%), and elevated liver enzymes (1.1%)
NS contains 154 mM Na+ and Cl-, with an average pH of 5.0 and osmolarity of 308 mOsm/L.
LR solution has an average pH of 6.5, is hypo-osmolar (272 mOsm/L), and has similar electrolytes (130 mM Na+, 109 mM Cl-, 28 mM lactate, etc.) to plasma
LR’s acid base balance is superior to that of NS’s
There were no significant differences between LR and NS groups in fibrinogen concentrations or platelet count
Total protein dropped
no significant differences in Hct (Table
1) or total protein between LR and NS groups
Bicarbonate HCO3- levels were decreased by hemorrhage but returned to pre-hemorrhage values by 3 h after LR resuscitation, whereas no return was observed with NS resuscitation
Na+ was increased after NS resuscitation
No changes in Na+ or K+ were observed
K+ did not change initially after NS resuscitation but was elevated at 6 h afterwards
Ca++ was similarly decreased
Cl- was elevated for 6 h after NS resuscitation, with no changes shown after LR resuscitation
PT was similarly prolonged by resuscitation with LR (from 11.2 ± 0.2 sec at baseline to 12.1 ± 0.2 sec at 6 h) and NS
Plasma aPTT was also similarly prolonged by resuscitation with LR (from 17.1 ± 0.5 sec baseline to 20.1 ± 1.2 sec at 6 h) or NS
NS resuscitation resulted in better oxygen delivery and oxygen delivery-to-oxygen demand ratio as an index of oxygen debt
NS had better tissue perfusion and oxygen metabolism than LR
LR resuscitation returned BE and bicarbonate to pre-hemorrhage levels within 3 h, but no return of BE or bicarbonate was observed for 6 hr with NS resuscitation
current blood bank guidelines state that LR should not be mixed with blood to prevent the risk of clot formation from calcium included in LR
LR resuscitation should not be given with blood through the same iv-line and crystalloids should be avoided in patients with blood transfusion
PT and aPTT were prolonged for 6 h after hemorrhage and resuscitation, suggesting a hypocoagulable states
potential thrombotic risk from LR resuscitation is unlikely.
we suspected that the blood pressure after NS resuscitation would be lower than that of LR due to its vasodilator effects
NS required a larger resuscitation volume and was associated with poor acid base status and elevated serum potassium in this model
NS required 50% more volume and was associated with a higher cardiac output and lower peripheral resistance, as compared to LR resuscitation
These differences are possibly due to the vasodilator effects from NS
an elevation of K+ was observed at 6 h post NS resuscitation, while no change of K+ was observed after LR resuscitation
The mechanism for the increase of K+ from NS is not fully known
NS is associated with vasodilator effects and the risks of metabolic acidosis and hyperkalemia