Retropharyngeal haematoma is a rare and potentially fatal cause of airway obstruction. The treatment of retropharyngeal haematoma is contentious. We report a case of an 84 year old woman on aspirin and warfarin who developed a retropharyngeal haematoma following minor blunt head and neck trauma. The patient presented insidiously with Capp’s triad and developed delayed airway obstruction necessitating emergency fibreoptic endoscopic intubation. Both tracheostomy and surgical drainage were avoided and she recovered well.
The influences of triiodothyronine (T3) or dopamine (DA) administration on growth, feed conversion, and visceral weights in broiler chicks between the ages of 6 and 12 d posthatch were investigated. In Trial 1, six chicks at age 6 d were randomly administered one of the following treatments: 0.37, 0.74, 1.48, and 2.96 micromol T3/kg BW or 0.07, 0.14, 0.28, and 0.56 micromol DA/kg BW. Both T3 and DA were administered via intraperitoneal injections between the end of sternum and the ends of os pubis, with 0.9% saline as the excepient. In addition, two groups of six birds each were either not injected or injected with excepient only, as controls. Four replications were carried out with a total of 264 chicks. Heart weight as a percentage of feed-deprived body weight (FDBW) of the chicks injected with 2.96 micromol T3/kg BW was heavier than that of controls. Other variables measured were not significantly different between treatments. In trial 2, six chicks at age 6 d were randomly administered, one of the following treatments: 0.56, 1.12, 2.24, and 4.48 micromol T3/kg diet or 0.40, 0.80, 1.60, and 3.20 micromol DA/kg diet as well as a nonsupplemented control. Four replications were carried out with 216 chicks. The results in Trial 2 showed that the effects of T3 (X, micromol/kg diet) on body weight gain (Y1, g) and feed consumption (Y2, g) were linear (Y1 = 310 - 21.5X, R2 = 0.868, P < 0.001 and Y2 = 398 - 22.3X, R2 = 0.765, P < 0.001, respectively). The feed conversion ratio, the weight of liver, the weights of various intestinal segments, the lengths of the duodenum, jejunum and the ileum, as well as weight per centimeter jejunal length, gizzard weight as percentage of FDBW, and the duodenal length per kilogram FDBW all had linear responses (P < 0.05) to the level of dietary supplementation of T3. The effect of dietary supplementation of T3 on the heart weight was quadratic (Y16 = 2.58 + 0.89X - 0.17 X2, R2 = 0.526, P < 0.01). Similarly, the weights of pancreas and gizzard, the heart weight as a percentage of FDBW and the pancreas weight as a percentage of FDBW all had second-order curve responses. Dietary DA supplementation exerted no effect on the variables measured except that the regression of the heart weight as a percentage of FDBW on dietary DA supplementation (X1, micromol/kg diet) existed, namely, Z1 = 0.64 + 0.24 X1 - 0.23 X1(2) + 0.05 X1(3) (R2 = 0.868, P < 0.05).
We report here that compound heterozygosity for hemoglobin Korle-Bu (HbKB) and HbC (beta 6 Glu-->Lys) is associated with moderate chronic hemolytic anemia with microcytosis. To understand the pathogenesis of this syndrome, we have studied the effect of Hb Korle-Bu (KB = beta 73 Asp-->Asn) on the crystallization of HbC. We have previously established that fetal Hb (HbF) inhibits the crystallization of HbC. In contrast, HbS accelerates crystallization affecting the pathogenesis of SC disease. We now report on in vitro crystallization of mixtures of HbKB, HbC, and various amounts of HbF and the native hemolysate of a child who is a compound heterozygote for HbKB and HbC. At 6 months of age, the propositus' hemolysate contained 55% HbKB, 39% HbC, and 6% HbF. Crystal formed within 2 minutes compared with 30 minutes for the mixture of 40% HbC:60% HbS and with 180 minutes for 40% HbC:60% HbA. The morphology of the crystals formed was cubic, in contrast with the tetragonal crystals observed in CC and SC disease. Early crystals did not exhibit “sharp edges” until 45 minutes. Purified HbKB formed aggregates but not crystals after 24 hours. Isopycnic gradients showed that the KB/C compound heterozygotes have red blood cell (RBC) densities intermediate between the AC and CC phenotype and similar to SC disease. The surface residue beta 73, known to participate in areas of interaction of the deoxy HbS polymer, can now be assigned to areas of contact in HbC containing crystals. The hemolysis observed in the HbKB/C compound heterozygote is likely to be secondary to the acceleration of Hb crystallization. The microcytosis and increased RBC density is clearly the consequence of the presence of HbC, but the basis of the increased RBC pathology compared with AC trait, despite the low proportion of HbC (35% to 40%), remains to be elucidated.
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