OBJECTIVE: To analyze the causes of misdiagnosis in patients with familial nasal bleeding and to improve the level of diagnosis and treatment. METHOD: The clinical characteristics of 7 families with nose blood were analyzed retrospectively and 2 typical cases were reported, including their treatment and misdiagnosis in consulting, out-patient and in-patient. RESULT: Typical case 1 was misdiagnosed and mistreated for 42 years, misdiagnosed as blood disease so that the patient was biopsied in bone marrow, misdiagnosed as endometriosis so that the patient was performed uterus resection. Typical case 2 was misdiagnosed and mistreated for 17 years, misdiagnosed as upper digestive tract hemorrhage so that the patient was performed endoscopic sleeve ligation, misdiagnosed as inferior turbinate hemangioma so that the patient was performed nasal endoscopic surgery. CONCLUSION Neglect of family history and the typical signs are the causes of misdiagnosis. So asking about the family history and checking for the typical signs in patients with nose blood can avoid misdiagnosis.
Diagnostic Errors ; Endoscopy ; Epistaxis ; diagnosis ; Female ; Humans ; Nasal Surgical Procedures ; Retrospective Studies ; Turbinates

Objective To study the effects of acetated ringer's solution resuscitation in hemorrhagic shock rats on inflammatory mediators on lung tissue and their JNK (c-Jun N-terminal kinase) signaling pathways. Methods Thirty-two SD rats were randomly(random number) divided into four groups: shock without resuscitation group (CR, n=8), saline group (NR, n=8), lactated ringer's solution group (LR, n=8) and acetated ringer's solution group (AR,n=8). The rats of NR group, LR group and AR group were prepared into shock models (mean arterial blood pressure maintained at 40-45 mmHg),The rats of NR group, LR group and AR group were in the shock for 60 min and then the corresponding kinds of liquid were administered for 30 min and observation was carried out for 4 hours. The rats of CR group without liquid resuscitation were observed for 4 hours after shock. After that, the lung tissues of rats were taken from NR group, LR group and AR group as well as from CR group 4 hours after shock (if the rats died, the lung tissues were immediately taken). The levels of TNF-α, IL-4 and IL-10 mRNA in lung were measured by real-time polymerase chain reaction (RT-PCR),and Western blot was used to measure the levels of JNK phosphorylation and MKP-1 acetylation. The one-way ANOVA was used for comparison among groups. Between the two groups, the comparison was analyzed by using LSD-t test. Results The IL-4 mRNA expression of lung tissue in AR group was higher than that in CR group, NR group and LR group (CR group:0.42±0.34; NR group:2.60±0.66; LR group:6.24±2.95; AR group: 11.08±4.24; P＜0.05).The IL-10 mRNA expression of lung tissue in AR group was significantly higher than that in CR group, NR group and LR group (CR group:0.25±0.25; NR group:2.79±1.62; LR group:3.51±1.66; AR group:9.35±2.86;P＜0.01).The TNF-a mRNA expression in AR group was significantly lower than that in CR group, NR group and LR group (CR group:4.98±1.26; NR group:2.50±0.76; LR group:3.87±3.00; AR group:0.19±0.09; P＜0.01). The level of JNK phosphorylation in lung tissue of rats in AR group was significantly lower than that in CR group, NR group and LR group (CR group:0.52±0.12; NR group:0.42±0.08; LR group:0.30±0.08; AR group:0.17±0.06;P＜0.01). The level of MKP-1 acetylation in lung tissue of rats in AR group was significantly higher than that in CR group, NR group and LR group (CR group:0.14±0.07; NR group:0.30±0.07; LR group:0.37±0.02; AR group:0.48±0.06;P＜0.01). Compared with normal saline and lactated ringer's solution, acetated ringer's solution used in hemorrhagic shock rats could promote MKP-1 acetylation, inhibit the phosphorylation of JNK, significantly inhibit the lung tissue TNF-a released, promote the release of anti-inflammatory factors, IL-4 and IL-10. Conclusions The acetated ringer's solution for resuscitation of hemorrhagic shock in rats could reduce inflammation of lung tissue in a certain extent, probably by enhanced the acetylation of MKP-1 to inhibited JNK signaling pathway and reduced lung tissue inflammation.

Objective To analyze the clinical values of super early enteral nutrition combined with microecopharmaceutics and delayed enteral nutrition on patients with severe acute pancreatitis. Methods Clinical data of thirty patients diagnosed as severe acute pancreatitis in our emergency department during January 2013 and December 2017 were reviewed retrospectively. Patients were divided into the treatment group (n=15, patients given enteral nutrition combined with microecopharmaceutics within 24 h after admission) and the control group (n=15, patients given delayed enteral nutrition after 48 h of admission). Two weeks after the treatment, the serum variables of C-reactive protein, total protein, albumin, recovery time of urine and blood amylase, length of hospital stay and APACHE Ⅱ score were compared between the two groups by using paired samples t test. Results The C-reactive protein [(46.7±13.1) mg/L vs. (190.72±19.3) mg/L, t=10.4, P<0.01] and APACHE Ⅱ score [(7.2±1.9) vs.(9.3±2.4),t=2.7,P<0.05] of the treatment group were significantly lower than those in the control group. The total protein [(58.1±6.3)g/L vs.(52.6±5.4)g/L, t=2.5, P<0.05] and albumin [(29.9±3.2)g/L vs.(22.0±2.8)g/L, t=7.12, P<0.01] of the treatment group were significantly higher than those in the control group. The recovery time of urine amylase [(13.2±2.1)d vs.(18.7±3.9)d, t=4.9, P<0.01] and blood amylase [(7.5±3.0)d vs.(11.1±3.4)d, t=3.1, P<0.01], and length of hospital stay[(14.9±4.5)d vs.(27.1±5.3)d, t=6.9, P<0.01] were significantly shorter in the treatment group compared with those in the control group. Conclusions Ultra-early enteral nutrition combined with microecopharmaceutics can shorten the length of hospital stay of patients with severe acute pancreatitis, and is safe and effective.

Objective To investigate the target blood pressure level of restrictive fluid resuscitation in patients with traumatic hemorrhagic shock. Methods Sixty patients with traumatic hemorrhagic shock admitted to the First Affiliated Hospital of Bengbu Medical College from January 2016 to December 2018 were enrolled. All patients were resuscitated with sodium acetate ringer solution after admission. According to the difference of mean arterial pressure (MAP) target, the patients were divided into low MAP (60 mmHg ≤ MAP < 65 mmHg, 1 mmHg = 0.133 kPa), middle MAP (65 mmHg ≤ MAP < 70 mmHg) and high MAP (70 mmHg ≤ MAP < 75 mmHg) groups by random number table using the admission order with 20 patients in each group. Those who failed to reach the target MAP after 30-minute resuscitation were excluded and supplementary cases were deferred. The restrictive fluid resuscitation phase was divided into three phases: before fluid resuscitation, liquid resuscitation for 30 minutes and 60 minutes. The most suitable resuscitation blood pressure level was further speculated by monitoring the inflammatory markers and hemodynamics in different periods in each group of patients. Pearson correlation analysis was used to detect the correlation of variables. Results Before fluid resuscitation, there was no significant difference in hemodynamics or expressions of serum cytokines among the three groups. Three groups of patients were resuscitated for 30 minutes to achieve the target blood pressure level and maintain 30 minutes. With the prolongation of fluid resuscitation time, the central venous pressure (CVP), cardiac output (CO) and cardiac index (CI) were increased slowly in the three groups, and reached a steady state at about 30 minutes after resuscitation, especially in the high MAP group and the middle MAP group. The expressions of serum inflammatory factors in the three groups were gradually increased with the prolongation of fluid resuscitation time. Compared with the low MAP group and the high MAP group, after 30 minutes of resuscitation the middle MAP group was superior to the other two groups in inhibiting the expressions of pro-inflammatory factors tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and promoting anti-inflammatory factors IL-10 [TNF-α mRNA (2-ΔΔCt):0.21±0.13 vs. 0.69±0.34, 0.57±0.35; IL-6 mRNA (2-ΔΔCt): 0.35±0.31 vs. 0.72±0.39, 0.59±0.42; IL-10 mRNA (2-ΔΔCt): 1.25±0.81 vs. 0.61±0.46, 0.82±0.53; all P < 0.05], but there was no significant difference in promoting the expression of IL-4 mRNA among three groups. At 60 minutes of resuscitation, compared with the low MAP group and the high MAP group, the middle MAP group could significantly inhibit the expressions of TNF-α, IL-6 and promote IL-10 [TNF-α mRNA (2-ΔΔCt): 0.72±0.35 vs. 1.05±0.54, 1.03±0.49; IL-6 mRNA (2-ΔΔCt): 0.57±0.50 vs. 1.27±0.72, 1.01±0.64; IL-10 mRNA (2-ΔΔCt): 1.41±0.90 vs. 0.81±0.48, 0.94±0.61; all P < 0.05]. Compared with the high MAP group, the middle MAP group had significant differences in promoting the expression of IL-4 mRNA (2-ΔΔCt: 1.32±0.62 vs. 0.91±0.60, P < 0.05). There was no significant difference in serum cytokine expressions at different time points of resuscitation between the low MAP group and the high MAP group (all P > 0.05). Correlation analysis showed that there was a strong linear correlation between MAP and mRNA expressions of TNF-α, IL-6, IL-10 in the middle MAP group (r value was 0.766, 0.719, 0.692, respectively, all P < 0.01), but had no correlation with IL-4 (r = 0.361, P = 0.059). Fitting linear regression analysis showed an increase in 1 mmHg per MAP, the expression of TNF-α mRNA increased by 0.027 [95% confidence interval (95%CI) = 0.023-0.031, P < 0.001], IL-6 mRNA increased by 0.021 (95%CI = 0.017-0.024, P < 0.001), and IL-10 mRNA increased by 0.049 (95%CI = 0.041-0.058, P < 0.001). Conclusions When patients with traumatic hemorrhagic shock received restrict fluid resuscitation at MAP of 65-70 mmHg, the effect of reducing systemic inflammatory response and improving hemodynamics is better than the target MAP at 60-65 mmHg or 70-75 mmHg. It is suggested that 65-70 mmHg may be an ideal target MAP level for restrictive fluid resuscitation.

OBJECTIVE: To investigate the effect of ulinastatin on the inflammatory mediators and their signaling pathways miR-146a/TLR4/NF-κB in rats with hemorrhagic shock. METHODS: Seventy-two SD rats were randomly assigned into shock without resuscitation group (SR group, =24), acetated Ringer's solution resuscitation group (AR group, =24) and ulinastatin treatment group (=24). In all the 3 groups hemorrhagic shock models were established by femoral artery bleeding (with the mean arterial pressure maintained at 30-40 mmHg) without resuscitation (in SR group) or with resuscitation (in AR and ulinastatin groups) using acetated Ringer's solution for 30 min at 60 min after the onset of shock. At 1, 4, and 6 h after the shock onset or immediately after shock if the rats died, the lung tissues were taken for measurement of mRNA expressions of miR-146a, tumor necrosis factor- (TNF-), interleukin-1 (IL-1), IL-4, IL-6 and IL-10 using real-time quantitative PCR and the protein expressions of TLR4, MyD88, IκB-, p-IκB-, NF-κB p65, IRAK4, p-IRAK4 (Thr345, Ser346), p-IRAK4 (Thr342) and TRAF6 using Western blotting. The lung histopathology of the rats was examined under optical microscope with HE staining. RESULTS: Compared with the SR group, the rats in the AR group showed slightly alleviated inflammatory infiltration in the lung tissues with significantly increased mRNA levels of miR-146a, IL-4 and IL-10 ( < 0.05) and protein expressions of IκB-, p-IRAK4 (Thr342) and p-IRAK4 (Thr345, ser346) ( < 0.05), and decreased mRNA levels of TNF-, IL-1 and IL-6 ( < 0.05) and protein expressions of TLR4, MyD88, NF-κB p65, p-IκB-, IRAK-4 and TRAF6 ( < 0.05). Compared with those in AR group, the rats in ulinastatin group showed further alleviation of inflammatory lung tissue injury, with increased mRNA levels of miR-146a, IL-4 and IL-10 ( < 0.01) and protein expressions of IκB-, p-IRAK4 and p-IRAK4 ( < 0.01) and decreased mRNA levels of TNF-, IL-1 and IL-6 ( < 0.01) and protein expressions of TLR4, MyD88, NF-κB p65, p-IκB-, IRAK-4 and TRAF6 ( < 0.01). CONCLUSIONS Ulinastatin combined with acetated Ringer's solution resuscitation alleviates lung inflammations in rats with hemorrhagic shock possibly by enhancing miR-146a expression to regulate TLR4/NF-κB signaling pathway through a negative feedback mechanism and thus modulate the balance of pro-inflammatory and anti-inflammatory factors.