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 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 8  |  Issue : 1  |  Page : 1-9

A study of arterial pH, bicarbonate levels, and base deficit at presentation as markers of predicting morbidity and mortality in acute pancreatitis


Department of Surgery, Jawaharlal Nehru Medical College Hospital, Aligarh Muslim University, Aligarh, Uttar Pradesh, India

Date of Web Publication14-Mar-2019

Correspondence Address:
Dr. Aditya Varshney
Department of Surgery, Jawaharlal Nehru Medical College Hospital, Aligarh Muslim University, Aligarh, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ais.ais_23_18

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  Abstract 


Background: The development of metabolic acidosis can occur commonly during critical illness. It is a clinical disturbance characterized by a low arterial pH, a reduced plasma HCO3 concentration, and compensatory hyperventilation. An extensive search for objective tools that predict severity and outcome at the time of hospital admission remains a major challenge.
Patients and Methods: Patients with acute pancreatitis presenting to our unit between January 2012 and November 2013 were prospectively studied. Arterial blood gas (ABG) analysis was done at admission, and development of organ failure, any need for intervention, and mortality were noted. The association between various parameters of ABG analysis and the development of organ failure or local complications, need for interventions (endoscopic/radiological/surgical), and mortality were analyzed.
Results: In all, 100 patients (mean age: 36.25 ± 12.86 years; 47.0% males and 53.0% females) were studied. The etiology of acute pancreatitis was Gall stone disease in 52 (52.0%), Alcoholism in 35 (35%), and others in 13 patients (13%). Of the 100 patients, acute fluid collections developed in 84 patients (84%). Multiple organ failure developed in 18 patients (18%). Respiratory failure developed in 68 patients (68%) and renal failure developed in 15 patients (15%), whereas 13 patients (13%) developed shock. Seven of the 19 patients (36.84%) with pH ≤7.35 died when compared with 1 of 81 patients (1.23%) with pH >7.35 (P = 0.001). Seven of the 58 patients (13.79%) with bicarbonate ≤24 mEq/L died when compared with 1 of 42 patients (2.38%) with bicarbonate >24 mEq/L (P = 0.05). Seven of 36 patients (19.4%) with base deficit ≥−4.0 died when compared with 1 of 64 patients (1.56%) with base deficit >4.0 (P = 0.002).
Conclusion: Low arterial pH, low bicarbonate levels, and higher base deficit at presentation predict an adverse outcome with more frequency of organ failure, need for intervention, and mortality.

Keywords: Acute pancreatitis, arterial blood gas, base deficit, bicarbonates, metabolic acidosis


How to cite this article:
Varshney A, Aslam M, Alam J. A study of arterial pH, bicarbonate levels, and base deficit at presentation as markers of predicting morbidity and mortality in acute pancreatitis. Arch Int Surg 2018;8:1-9

How to cite this URL:
Varshney A, Aslam M, Alam J. A study of arterial pH, bicarbonate levels, and base deficit at presentation as markers of predicting morbidity and mortality in acute pancreatitis. Arch Int Surg [serial online] 2018 [cited 2019 Mar 26];8:1-9. Available from: http://www.archintsurg.org/text.asp?2018/8/1/1/254143




  Introduction Top


Acute pancreatitis is an inflammatory process of the pancreas that can be localized, involve regional and distant organs, or cause overwhelming illness or death. While the exact etiology and mechanisms of acute pancreatitis are still controversial, 70%–80% of cases are caused by alcohol abuse and common bile duct obstruction with gallstones.[1] It is thought that an initial insult to the pancreas causes the premature activation of digestive enzymes, mainly trypsin found in the organ's acinar cells. When inappropriately activated, trypsin causes pancreatic inflammation and autodigestion, which can cause a release of amylase and lipase into the serum. In severe cases, this release of trypsin can mediate the release of other proinflammatory cytokines such as tumor necrosis factor-α and proteolytic enzymes into the circulation resulting in pancreatic necrosis, systemic inflammatory response syndrome, septic shock, and multiorgan failure.[2] Because it is important to predict the severity of the illness as early as possible to optimize the therapy and to prevent organ dysfunction and local complications, several scores of severity have been proposed. Criteria of severity such as Ranson,[3] Glasgow,[4] Acute Physiology and Chronic Health Evaluation II (APACHE-II),[5] Balthazar score,[6] or computed tomography severity index scores have been used for a long time. These scores assess the multiple organ dysfunction induced by the disease, and consequently, the greater the number of organs injured, the greater the score.[7]

Serum amylase and lipase have long been used as a marker for pancreatitis. Serum amylase is increased in 85% of patients in the first day of symptoms and remains elevated for 3–5 days in uncomplicated cases. Greater than three-fold rise in amylase is considered conclusive. The sensitivity and specificity are 78.6% and 99.1%, respectively. Serum lipase, on the other hand, has a sensitivity and specificity for diagnosing pancreatitis of 96.4% and 99.6%, respectively.[8]

The development of metabolic acidosis can occur commonly during critical illness. It is a clinical disturbance characterized by a low arterial pH, a reduced plasma HCO3 concentration, and compensatory hyperventilation. Severe metabolic acidosis represents detrimental clinical effects including hyperventilation, decreased cardiac contractility and cardiac output, cardiac arrhythmia, pulmomary edema with minimal volume overload, and depressed central nervous system function.[9]

Metabolic acidosis has been one of the criteria used for predicting a severe course of acute pancreatitis; it is one of the factors measured within 48 h of admission as a part of Ranson's scoring system.[10] Arterial pH is also a component of the APACHE-II scoring system that is commonly used in acute pancreatitis.[5] Metabolic acidosis can occur in acute pancreatitis for multiple reasons that include lactic acidosis resulting from shock, renal failure, or late in the course of disease because of loss of bicarbonate-rich pancreatic secretions due to pancreatic duct disruption.[10]

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection.[11] Septic shockis a subset of sepsis with circulatory and cellular/metabolic dysfunction associated with a higher risk of mortality.[12] The guidelines from the Surviving Sepsis Campaign emphasize using lactate levels to diagnose patients with sepsis-induced hypoperfusion.[13] The normal lactate level is less than 2 mmol/L.[14] Patients who presented with lactate values greater than 4 mmol/L with or without hypotension are significantly associated with mortality and are associated with a significantly higher risk than intermediate levels (2–4 mmol/L).[15]

With the limitation of all scoring systems, early prognosis in severe acute pancreatitis subjects has been a tough task. An extensive search for objective tools that predict severity and outcome at the time of hospital admission remains a major challenge.

  • This study will evaluate arterial pH, bicarbonate levels and base deficit on admission in patients with acute pancreatitis
  • It will determine their value in predicting organ failure, local complications, need for surgery or intervention, and mortality.



  Patients and Methods Top


This prospective study was conducted at the Department of Surgery, Jawaharlal Nehru Medical College Hospital, AMU, Aligarh, India, between October 2015 and September 2017 with an aim to evaluate arterial pH, bicarbonate levels, and base deficit on admission in patients with acute pancreatitis and to study their value in predicting organ failure, local complications, need for surgery or intervention, and mortality. For this purpose, a total of 100 patients with acute pancreatitis were enrolled in the study.

Inclusion criteria

Patients (age >14 years) with acute pancreatitis who presented within 10 days after the onset of pain are included in this study. Any two of the three criteria are to be fulfilled to diagnose acute pancreatitis:

  1. Clinical signs and symptoms suggestive of pancreatitis (acute-onset upper abdominal pain with or without radiation to back, vomiting, constipation, and obstipation)
  2. Elevated serum amylase/lipase to greater than three times the upper limit of normal
  3. Positive abdominal imaging.


Exclusion criteria

  • Patients who do not give consent for participation.
  • Patients with coronary artery disease/preexisting cardiac disorder.
  • Patients with diabetes mellitus, renal failure, malignancy, pregnancy, and chronic obstructive pulmonary disease.
  • Patients having underlying chronic pancreatitis and pancreatic malignancy.
  • Patients having underlying acid–base disorder.
  • Patients who presented >10 days after onset of pain.


Sample collection

  • For arterial blood gas (ABG) analysis, 1–2 mL of blood was collected from artery (radial/brachial/femoral) into heparinized syringe on the day of admission and immediately analyzed using the GEM premier 3000 analyzer [Figure 1], and the report was received and analyzed [Figure 2].
Figure 1: GEM premier 3000 analyzer

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Figure 2: Report received from analyzer

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The analysis included measurement of arterial pH, partial pressure of arterial carbon dioxide (PaCO2), partial pressure of arterial oxygen (PaO2), and blood lactate levels. Standard bicarbonate (HCO3) and base deficit/excess (BD/E), which represents the amount of acid or base required to normalize the pH in a liter of blood, were directly calculated by the blood gas analyzer (GEM premier 3000 analyser) as applied to a standard normogram.

These patients were followed up to clinical recovery or death. The associations between various parameters of ABG analysis and development of organ failure or local complications, need for interventions (endoscopic/radiological/surgical), and mortality were analyzed.

Statistical analysis

All the data were compiled on Microsoft Office Excel 2007®. Descriptive data were presented as percentages for categorical variables and mean ± standard deviation for quantitative variables. The patients were categorized into subgroups based on the arterial pH (pH ≤7.35 and >7.35), bicarbonate levels (≤24 and >24 mEq/L), and base deficit values (≥−4 and <−4 mEq/L). Data were subjected to statistical analysis with the help of SPSS 20® software. The continuous variables were compared using a Student's t-test, whereas the categorical variables were compared using Chi-square test. Statistical significance was accepted when P value was ≤0.05.


  Observations and Results Top


A total of 100 patients with acute pancreatitis were enrolled in the study. Of 100 patients enrolled, 47 (47%) were males and 53 (53%) were females. The mean age of the patients included was 36.25 ± 12.86 years (range: 19–62 years) [Table 1], [Figure 3]. The etiology of acute pancreatitis was gall stone disease in 52 patients (52%), alcoholism in 35 patients (35%), and others in 13 patients (13%). The other etiologies were post ERCP in three patients, post laparoscopic cholecystecomy in one patient, trauma in three patients, hyperlipidemia in one patient, hypercalcemia in two patients, and drug-induced in one patient (the patient was taking sodium valproate for epilepsy). The mean period from onset of symptoms to presentation at our hospital was 3.54 ± 1.68 days [Table 2], [Table 3] and [Figure 4], [Figure 5].
Table 1: Demographic profile of the patients

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Figure 3: Pie chart showing sex distribution of patients

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Table 2: Etiology of acute pancreatitis

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Table 3: Other causes of acute pancreatitis

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Figure 4: Bar diagram showing etiology of acute pancreatitis

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Figure 5: Bar diagram showing other causes of acute pancreatitis

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In this study, of 100 patients, acute fluid collections developed in 84 patients (84%). Multiple organ failure developed in 18 patients (18%). Respiratory failure developed in 68 patients (68%) and renal failure developed in 15 patients (15%), whereas 13 patients (13%) developed shock. Interventions including percutaneous and endoscopic interventions as well as surgery were needed in 18 patients (18%) [Table 4], [Figure 6] and mortality occurred in 8 patients (8%).
Table 4: Details of interventions

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Figure 6: Bar diagram showing details of intervention done in patients of acute pancreatitis

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ABG parameters

In this study, the mean arterial pH was 7.38 ± 0.08, and pH ≤ 7.35 was present in 19 patients (19%). The mean arterial bicarbonate level was 23.16 ± 7.82 mEq/L, with 58 patients (58%) having values ≤24 mEq/L. Base deficit more than −4 mEq/L was found in 36 (36%) patients.

Association of arterial pH with various outcome parameters

The patients with evidence of pH ≤7.35 had a higher frequency of organ failure (respiratory failure and renal failure), multiple organ failure, shock, and greater need for intervention. Multiple organ failure was present in 18 patients, 7 of whom had pH ≤7.35 (P = 0.01). Of 13 patients in whom shock was present, 6 patients had arterial pH ≤7.35 (P = 0.001). Interventions were required in 18 patients. Seven patients from the group with pH ≤ 7.35 needed intervention, compared with 11 patients from the second group (P = 0.01). Eight patients with arterial pH ≤ 7.35 died, whereas one patient with pH value >7.35 died, and this difference was statistically significant (P = 0.001) [Table 5].
Table 5: Association of arterial pH with various outcome parameters

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Association of arterial bicarbonates (HCO3) with various outcome parameters

We compared outcomes in the two bicarbonate groups, that is, those with arterial HCO3 ≤24 versus those >24 mEq/L. Multiple organ failure was present in 18 patients, 15 of whom had bicarbonate ≤24 mEq/L (P = 0.05); 10 of 13 patients with shock had bicarbonate ≤24 mEq/L (P = 0.018). Respiratory failure was present in 68 patients and 44 of these had bicarbonate levels ≤24 mEq/L (P = 0.04). Of the 15 patients who had renal failure, 13 had bicarbonate levels ≤24 mEq/L (P = 0.01). Intervention was required in 14 of 58 patients with bicarbonate ≤24 mEq/L (P = 0.09). Of eight deaths reported in this study, seven had bicarbonate ≤24 mEq/L. The mortality was significantly higher in patients with low bicarbonate levels (P = 0.05) [Table 6].
Table 6: Association of arterial bicarbonates (HCO3-) with various outcome parameters

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Association of arterial base deficit with various outcome parameters

A total of 36 patients had base deficit ≥−4, whereas 64 patients had base deficit <−4 mEq/L. Multiple organ failure was seen in 18 patients and 12 of these had base deficit ≥−4 mEq/L (P = 0.01). Of the 13 patients with shock, 9 patients had base deficit ≥−4 mEq/L (P = 0.007). Respiratory failure was present in 27 patients with base deficit ≥ 4 meq/L and was present in 41 patients in the second group. This difference between the two groups was not significant (P = 0.26). Of the 15 patients who had renal failure, 12 were in the greater base-deficit group (P = 0.001). Eight patients with base deficit ≥−4 mEq/L required intervention, when compared with 10 patients with lower base deficit and the difference did not reach statistical significance (P = 0.29). Seven deaths in this study occurred in patients with base deficit ≥−4 mEq/L, compared with one death in the second group. The mortality was significantly higher in these patients with base deficit ≥−4 mEq/L (P = 0.002) [Table 7]. Therefore, low pH, low bicarbonates, and higher base deficit show a significant association with mortality [Table 8], [Table 9], [Table 10].
Table 7: Association of arterial base deficit with various outcome parameters

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Table 8: Association of arterial pH with mortality

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Table 9: Association of arterial bicarbonates (HCO3-) with mortality

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Table 10: Association of arterial base deficit with mortality

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  Discussion Top


There have been a number of scoring and classification systems proposed for assessment of acute pancreatitis that a clinician is often confused, hence there is always a need for an objective criteria through which a clinician could assess the severity of the disease and assess its complications.[16] In the recent years, researchers have proposed the use of ABG parameters and its role in predicting severe acute pancreatitis.[10]

In this study, we made an attempt to find out associations of ABG parameters with severity of acute pancreatitis. For this purpose, a prospective study was carried out in which a total of 100 patients of acute pancreatitis were enrolled to predict severity and outcomes in terms of local complications, organ failure, need for surgery or intervention, and mortality.

Although multiple scoring systems and single markers are being used for predicting an outcome in acute pancreatitis, there is no consensus regarding the use of one or the other in clinical practice. ABG parameters have not been evaluated for prediction of severity and outcome in acute pancreatitis, even though individual parameters form components of multiscore assessment such as Ranson's[3] and APACHE II scoring system.[5],[17] In fact, one of the report criticized ABG analysis as an unnecessary tool in patients with acute pancreatitis. This report, unfortunately, focused primarily on the blood gas and oxygenation-related parameters such as PaO2.[18] In other critical illnesses, there is sufficient evidence to implicate ABG parameters as important predictors of severity and outcomes.[19]

It has been observed that patients with organ failure at admission have higher mortality than those who do not. The development of organ failure, whether at admission or thereafter, implies a worse prognosis. The highest mortalities are among patients with multiple and persistent organ failure.[20]

In this study, 18 patients suffered multiple organ failure which was present in 7 of the 19 patients (36.84%) with pH levels ≤7.35, and this frequency was significantly higher than the patients group with pH >7.35 (13.58%; P = 0.01). Also, 15 of the 42 patients (25.86%) with bicarbonate ≤24 mEq/L developed multiple organ failure in contrast to 3 of the 42 patients (7.14%) with a bicarbonate level >24mEq/L (P = 0.05). Twelve of the 36 patients (33.33%) with an arterial base deficit ≥−4.0 suffered multiple organ failure which was significantly more than the patients' group with an arterial base deficit <−4.0 (9.37%; P = 0.01). The association between acidosis and an increase in multiple organ failure and mortality for intensive care patients has long been known.[21]

Early multiple organ dysfunction syndrome (MODS) in the first week is a major cause of death in patients with acute pancreatitis.[22] An audit[23] of all patients of acute pancreatitis (n = 13,727) in Scotland from 1984 to 1995 found that 54% of deaths occurred during the first week. There is an agreement with an autopsy series[24] and other prospective studies;[25],[26],[27] some reports describe infected pancreatic necrosis which normally features later in the second or third week as the major cause of death.[28] Early MODS also represents the most important nonfatal complication of acute pancreatitis, causing major morbidity and a strain on resources.[29]

In this study, interventions were required in 18 patients [in 9 patients ultrasound-guided percutaneous catheter drain (PCD) was inserted, in 4 patients endoscopic retrograde cholangiopancreatography (ERCP) was done, in 2 patients transgastric debridement with internal drainage (cystogastrostomy) was done, in 1 patient necrosectomy was done, in 1 patient necrosectomy plus cholecystectomy was done].

Seven of the 19 patients (36.84%) with pH ≤7.35 underwent interventions when compared with 11 of the 81 patients (13.58%) with pH >7.35 (P = 0.01) showing the need for intervention was significantly more in patients with arterial pH ≤7.35 (P = 0.01). Intervention was required in 14 of 58 patients (24.14%) with bicarbonate ≤24 mEq/L when compared with 4 of 42 patients (P = 0.09). This did not show significant association with low bicarbonate. Although studies of factors on admission that predict the need for intervention are scant.

A retrospective study[30] with 276 patients with acute pancreatitis concluded that it was difficult to determine the subgroup of patients likely to develop significant pancreatic necrosis. About 61% of patients completely settled with conservative treatment. In the rest, intervention was required for better outcome in patients with pancreatic necrosis and in patients who were dealing with complications of necrosis such as multiple organ failure. In our study, intervention was done in 18% of patients.

A meta-analysis by the Dutch Pancreatitis Study Group,[31] which included 384 patients, reported that the presence of organ failure and infected pancreatic necrosis could predict the need for intervention. A subset of patients among those managed by the step-up approach will still require surgery.

A prospective study[32] included 70 consecutive patients with severe acute pancreatitis to identify factors that could predict surgical intervention after initial management with PCD. Reversal of sepsis within a week after PCD, APACHE II score at first intervention, and multiple organ failure within a week of the onset of disease could predict the need for surgery in the early course of disease. The number of patients with metabolic acidosis and higher base deficit at admission was significantly higher in the pancreatic necrosectomy group, compared with the PCD-alone group.

In this study, 7 of the 19 patients (36.84%) with pH ≤ 7.35 died when compared with 1 of 81 patients (12.34%; P = 0.001), and 13.79% of patients with bicarbonate ≤24 mEq/L (P = 0.05) and 19.4% of patients with base deficit ≥−4 mEq/L (P = 0.002) also succumbed to their illnesses. Studies in intensive care settings have documented the effects of metabolic acidosis on mortality.

In a Brazilian study,[33] metabolic acidosis (bicarbonate level of less than 18 mEq/L) was seen in 23 of 71 patients with acute pancreatitis (32%), and mortality was reported in 15 of 23 patients (65.21%). In our study, pH of 19 patients was ≤7.35, and mortality was reported in 7 patients (36.84%).

In a prospective study[34] of 279 patients with acute pancreatitis, mortality was reported in 17 patients (6.09%) and mortality was 10-fold higher in patients having multiple organ failure. In our study, multiple organ failure developed in 18 patients (18%) and mortality occurred in 8 patients (8%).

A study[35] of 107 patients admitted to the intensive care unit (ICU) for various reasons demonstrated a significantly severe metabolic acidosis in nonsurvivors. Another study[36] reported that severe metabolic acidosis (arterial blood pH ≤7.20) occurred within the first 24 h in the ICU in 6% of critically ill patients and was associated with high rates of mortality in patients admitted to ICU.

In a prospective, observational study[37] of a large cohort of 530 patients, pH at presentation predicted not only long-term mortality but also ICU admission, in-hospital mortality, and mortality after 30-day follow-up. Patients with a pH level of ≤7.39 showed a mortality rate of 37% after 12 months. In our study, mortality rate was 36.84% in patients with pH ≤7.35.

Although many parameters including serum creatinine, hematocrit, obesity, blood urea nitrogen, C-reactive protein, and serum procalcitonin have been studied previously to predict severity and outcome in patients with acute pancreatitis,[38] this study is important because a detailed evaluation of ABG parameters in patients with acute pancreatitis has not previously been reported. Our results suggest that low pH, low bicarbonate, and higher base deficit at presentation predict an adverse outcome and worse prognosis in patients with acute pancreatitis, including the occurrence of organ failure, need for intervention, and mortality. Therefore, carrying out an ABG in patients with acute pancreatitis not only helps in management of patients but also may predict the outcome.


  Summary and Conclusion Top


The observations are summarized as follows:

  1. Of the 100 patients, pH value was ≤7.35 in 19 patients (19%), bicarbonate was ≤24 mEq/L in 58 patients (58%), and base deficit ≥−4 mEq/L was found in 36 patients (36%)
  2. Of the 100 patients, acute fluid collection was developed in 84 patients (84%), multiple organ failure was developed in 18 patients (18.0%), respiratory failure was developed in 68 patients (68%), and renal failure was developed in 15 patients (15%), whereas 13 patients (13%) developed shock. Interventions including percutaneous and endoscopic interventions as well as surgery were needed in 18 patients (18%), and mortality was reported in 9 patients (9%)
  3. 84 of the 100 patients developed acute fluid collection in our study. 16 of the 19 patients (84.21%) with pH levels ≤7.35 when compared with 68 of the 81 patients with pH >7.35 (13.58%) developed acute fluid collection (P = 0.978). 49 of the 58 patients (84.48%) with bicarbonate ≤24 mEq/L developed acute fluid collection in contrast to 35 of 42 patients (83.33%) with a bicarbonate level >24 mEq/L (P = 0.877). 31 of the 36 patients (86.11%) with an arterial base deficit ≥−4.0 developed acute fluid collection when compared with 53 of the 64 patients with base deficit <−4.0 (82.81%; P = 0.66). Therefore low pH, low bicarbonates, and higher base deficit did not show a significant association with acute fluid collection
  4. 18 of the 100 patients suffered multiple organ failure, which was present in 7 of the 19 patients (36.84%) with pH levels ≤7.35 when compared with 11 of the 81 patients with pH >7.35 (13.58%; P = 0.01). 15 of the 58 patients (25.86%) with bicarbonate ≤24 mEq/L developed multiple organ failure, in contrast to 3 of the 42 patients (7.14%) with a bicarbonate level >24 mEq/L (P = 0.05). 12 of the 36 patients (33.33%) with an arterial base deficit ≥−4.0 suffered multiple organ failure, which was significantly more than the patients' group with base deficit <−4.0 (9.37%; P = 0.01). Therefore, low pH, low bicarbonates, and higher base deficit show a significant association with multiple organ failure
  5. Interventions were required in 18 of the 100 patients in our study. Seven of the 19 patients (36.84%) with pH ≤7.35 underwent interventions when compared with 11 of the 81 patients (13.58%) with pH >7.35 (P = 0.01). This showed significant association with low pH. Fourteen of the 58 patients (24.14%) with bicarbonates ≤24 mEq/L underwent interventions when compared with 4 of the 42 patients (9.52%) with bicarbonate >24 mEq/L (P = 0.09). This did not show significant association with low bicarbonate. Eight of the 36 patients (22.22%) with base deficit ≥4.0 underwent interventions when compared with 10 of the 64 patients (15.62%) with base deficit >4.0 (P = 0.29). This did not show significant association with higher base deficit
  6. Eight deaths (8%) were reported out of 100 patients in our study. Seven of the 19 patients (36.84%) with pH ≤7.35 died when compared with 1 of the 81 patients (1.23%) with pH >7.35 (P = 0.001). Seven of the 58 patients (13.79%) with bicarbonate ≤24 mEq/L died when compared with 1 of the 42 patients (2.38%) with bicarbonate >24 mEq/L (P = 0.05). Seven of the 36 patients (19.4%) with base deficit ≥−4.0 died when compared with 1 of the 64 patients (1.56%) with base deficit >4.0 (P = 0.002). Therefore, low pH, low bicarbonates, and higher base deficit show a significant association with mortality
  7. The conclusion of our study is that in patients with acute pancreatitis, low arterial pH, low bicarbonate levels, and higher base deficit at presentation predict an adverse outcome with more frequency of organ failure, need for intervention, and mortality. Thus, a simple diagnostic analysis of ABG in patients with acute pancreatitis can help in predicting adverse outcome.


Financial support and sponsorship

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Conflicts of interest

There are no conflicts of interest.



 
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    Figures

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