Page 21 - Acute Pancreatitis (Viêm tụy cấp)

912 PART VII Pancreas

increasing oxygen requirements, intravenous fluids for maintain- Respiratory Care
ing the blood pressure, or renal replacement therapy) are indica-
tions for ICU or step-up unit care. Because of the common and indolent nature of hypoxemia affect-
ing patients with AP, current guidelines recommend the initial
Intravenous Fluid and Electrolyte Resuscitation routine use of nasal cannula oxygen in all patients with AP. 287
Supplemental oxygen, ideally by nasal prongs or by face mask
As the inflammatory process progresses early in the course of if needed, is given to maintain oxygen saturations well over 90%.
the disease, there is an extravasation of protein-rich intravascular If nasal or face mask oxygen fails to correct hypoxemia or if there
fluid into the peritoneal cavity and retroperitoneum, resulting in is fatigue and borderline respiratory reserve, noninvasive posi-
hemoconcentration and decreased renal perfusion with the asso- tive pressure ventilation or endotracheal intubation and assisted
ciated elevation in the BUN level and, later, the serum creatinine mechanical ventilation are required early.
level. Subsequently, the decreased perfusion pressure into the US of the nondependent lung can reliably detect evolving
pancreas leads to microcirculatory changes that result in pancre- respiratory dysfunction in AP. This simple bedside technique
atic necrosis. Thus an admission hematocrit of more than 44% shows promise as an adjunct to severity stratification. 288 ARDS
and a failure of the admission hematocrit to decrease at 24 hours is associated with severe dyspnea, progressive hypoxemia, and
have been shown to be predictors of necrotizing pancreatitis, 280 increased mortality. It generally occurs between the second and
and an elevation and/or rising BUN is associated with increased seventh day of illness (but can be present on admission) and con-
mortality. 272 The relationship of hematocrit and BUN, markers sists of increased alveolar capillary permeability causing inter-
of intravascular volume, to severity of AP implies that the oppo- stitial edema. Chest radiography may show multilobar alveolar
site is also true. Early vigorous IV volume repletion for the pur- infiltrates. Treatment is endotracheal intubation with positive
pose of intravascular resuscitation is of foremost importance. The end-expiratory pressure ventilation, often with low tidal volumes
goal is to provide enough intravascular volume to decrease the to protect the lungs from volutrauma. No specific treatment will
hematocrit and the BUN, thereby increasing pancreatic perfu- prevent or resolve ARDS. Noninvasive positive pressure ven-
sion. This is one of the extensively studied management strate- tilation in the early phases of ARDS 288 and continuous renal
gies in AP over the years. Intravenous volume administration has replacement therapy have also been reported to be useful in the
been widely recommended by experts and in various guidelines, treatment of ARDS in AP. 289 After recovery, pulmonary struc-
although there is significant variation in the various aspects of ture and function usually return to normal.
such intravenous volume administration in these guidelines and
reviews. 9,211,280-282 Haydock et al. in a systematic review observed Cardiovascular Care
that the level of evidence of such an important area in the man-
agement is at best very poor. 283 The various aspects of such intra- Cardiac complications of severe AP include heart failure, myo-
venous volume administration include the type of fluid, total cardial infarction, cardiac dysrhythmia, and cardiogenic shock.
amount given, rate, timing, duration, and the weight to moni- An increase in cardiac index and a decrease in total peripheral
tor the therapy. It not surprising that a national survey in New resistance may be present and respond to infusion of crystalloids.
Zealand found that there is significant variation in intravenous If hypotension persists even with appropriate fluid resuscitation,
volume administration in AP, that aggressive volume administra- intravenous vasopressors may be required.
tion is prescribed mostly for organ failure and there is no adher-
ence to the published guidelines. 284 Lactated Ringer solution is Metabolic Complications
supposed to reduce intracellular acidosis in the pancreas and thus
the tryptic activity. A small RCT showed a benefit with lactated Hyperglycemia may present during the first several days of severe
Ringer solution over normal saline with regards to a decrease in pancreatitis but usually disappears as the inflammatory process
SIRS score as well as CRP levels, but not in any of the important subsides. Blood sugars fluctuate, and insulin should be admin-
clinical outcomes. 285 istered cautiously. Leptin levels were associated with persistent
An AGA technical review 237 reported the meta-analysis of hyperglycemia early in the course of AP in one study from New
many eligible studies on the role of intravenous volume admin- Zealand. 290 Hypocalcemia is mainly due to a low serum albumin.
istration therapy in the early management of AP as follows: Serum albumin is lost as albumin-rich intravascular fluid extrava-
“In conclusion, there is insufficient evidence to state that goal- sates into peritoneum and retroperitoneum, as well as the nega-
directed therapy, using various parameters to guide fluid admin- tive phase reactant effect on reducing albumin synthesis during
istration, reduces the risk of persistent single or multiple organ the acute illness phase. This albumin loss causes a decrease in
system failure, infected (peri-) pancreatic necrosis or mortality the calcium normally bound to the albumin. Because this loss is
from AP. There is also no RCT evidence that any particular type nonionized, hypocalcemia is largely asymptomatic and requires
of fluid therapy (e.g., lactated Ringer’s) reduces the risk of mor- no specific therapy. However, reduced ionized serum calcium
tality or persistent single or multiple organ failure. The addition may occur and cause neuromuscular irritability. If hypomagne-
of hydroxyethyl starch to usual intravenous fluids does not reduce semia coexists, it inhibits the release of parathyroid hormone;
the risk of mortality, and may increase the risk of persistent mul- magnesium replacement should restore serum calcium to nor-
tiple organ system failure in AP.” Based on this meta-analysis, the mal in such instances. Causes of magnesium depletion include
accompanying AGA guidelines suggested goal directed therapy loss of magnesium in the urine, stool, or vomitus or deposition
for fluid management but cautioned the quality of evidence is of magnesium in areas of fat necrosis. Once the serum magne-
very low and future trials have to address the various aspects of sium is normal, signs or symptoms of neuromuscular irritability
such therapy in the early management of AP. 286 Despite these may require administering IV calcium gluconate, as long as the
limitations for practical purposes, one could suggest a fluid rate of serum potassium is normal and digitalis is not being given. IV
5 to 10 mL per kilogram body weight per hour or 250 to 500 mL calcium increases calcium binding to myocardial receptors, which
per hour of probably lactated Ringer solution, preferably during displaces potassium and may induce a serious dysrhythmia.
the first 24 hours after admission. Besides clinical monitoring for
volume overload, hourly urine output, decreases in hematocrit Antibiotics
and BUN/serum creatinine levels may be used for directing such
therapy with very minimal need for invasive monitoring. Agents Antibiotics are sometimes given in AP as prophylactic antibi-
like hydroxyethyl starch should not be used. otics (before a documented infection) or for the treatment of