Quadrilateral space syndrome (QSS) is a rare nerve entrapment disorder that occurs when the axillary nerve and posterior circumflex humeral artery (PCHA) become compressed in the quadrilateral space. QSS presents as vague posterolateral shoulder pain that is exacerbated upon the abduction and external rotation of the shoulder. Diagnosis of QSS is difficult because of the vague presentation of QSS. In addition, even though MRI and MR angiography can be used in QSS diagnosis, there is currently no “gold standard” diagnostic imaging studies for QSS. In this case report, we describe a novel ultrasound-guided technique for a diagnostic quadrilateral space block and present a case where the diagnostic block was used to diagnose QSS. We believe that a diagnostic block of the quadrilateral space is a useful adjunct in the evaluation of patients with suspected QSS, especially in cases where examination findings and other diagnostic modalities are indeterminate.

Platelet‐activating factor (PAF) acting via its receptor (PAFR) is implicated in the pathogenesis of persistent pulmonary hypertension of the newborn (PPHN). Effects of long‐term oxygen therapy on newborn lung are not well understood; therefore, we studied the effect of oxygen tension on ovine newborn pulmonary artery smooth muscle cells (NBPASMC). Our global hypothesis is that PPHN results from failure of newborn lamb pulmonary system to downregulate PAFR activity or to upregulate vasodilatory cyclic nucleotides (Cnucs) activity. NBPASMC from newborns 6–12 days old were studied in vitro at three different oxygen tensions (pO 2, [Torr]: hypoxia, <40; normoxia, 80–100; and hyperoxia, >100 Torr often clinically imposed upon newborns with PPHN). PAFR‐ and Cnucs mediated effects were determined. PAFR and PKA Cα mRNA expression as well as prostacyclin, thromboxane, cAMP production, and DNA synthesis was studied to assess PAFR‐mediated hypertrophy and/or hyperplasia. Hypoxia and hyperoxia increased specific PAFR binding. PAF treatment during hyperoxia increased PAFR gene, but decreased PKA‐Cα gene expression. Hypoxia and hyperoxia increased NBPASMC proliferation via PAFR signaling. Baseline prostacyclin level was ninefold greater than in fetal PASMC, whereas baseline thromboxane was sevenfold less suggesting greater postnatal cyclooxygenase activity in NBPASMC. PAF decreased, while forskolin and 8‐Br‐cAMP increased cAMP production. Decrease of PAFR effects by Cnucs indicates that normal newborn PA physiology favors vasodilator pathways to minimize PAF‐induced hypertrophy or hyperplasia. We speculate that failure of newborn lung to anchor downregulation of vasoconstrictors with upregulation of vasodilators leads to PPHN.

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