Reduced Blood Oxygen Research Articles

Commercial smartwatch with pulse oximeter detects short-time hypoxemia as well as standard medical-grade device: Validation study.

ObjectiveWe investigated how a commercially available smartwatch that measures peripheral blood oxygen saturation (SpO2) can detect hypoxemia compared to a medical-grade pulse oximeter.MethodsWe recruited 24 healthy participants. Each participant wore a smartwatch (Apple Watch Series 6) on the left wrist and a pulse oximeter sensor (Masimo Radical-7) on the left middle finger. The participants breathed via a breathing circuit with a three-way non-rebreathing valve in three phases. First, in the 2-minute initial stabilization phase, the participants inhaled the ambient air. Then in the 5-minute desaturation phase, the participants breathed the oxygen-reduced gas mixture (12% O2), which temporarily reduced their blood oxygen saturation. In the final stabilization phase, the participants inhaled the ambient air again until SpO2 returned to normal values. Measurements of SpO2 were taken from the smartwatch and the pulse oximeter simultaneously in 30-s intervals.ResultsThere were 642 individual pairs of SpO2 measurements. The bias in SpO2 between the smartwatch and the oximeter was 0.0% for all the data points. The bias for SpO2 less than 90% was 1.2%. The differences in individual measurements between the smartwatch and oximeter within 6% SpO2 can be expected for SpO2 readings 90%–100% and up to 8% for SpO2 readings less than 90%.ConclusionsApple Watch Series 6 can reliably detect states of reduced blood oxygen saturation with SpO2 below 90% when compared to a medical-grade pulse oximeter. The technology used in this smartwatch is sufficiently advanced for the indicative measurement of SpO2 outside the clinic.Trial RegistrationClinicalTrials.gov NCT04780724

Risk factors for death in patients with severe COVID-19 admitted to an intensive care unit

Aim. Severe COVID-19 is accompanied by reduced blood oxygen saturation, systemic inflammatory response syndrome and multiple organ failure, all causing a significant deterioration of homeostasis associated with death. Here we aimed to study the risk factors for death in patients with severe COVID-19 who have been admitted to an intensive care unit.Materials and Methods. The study included 144 consecutive patients with severe COVID-19 who have been admitted to an intensive care unit of Kuzbass Clinical Hospital from August to December 2020. Groups of survivors and non-survivors were equal in number (n = 72) and matched by gender (36 men and women) and age (median age 64 years, interquartile range 56-70 years in survivors and 58-69 years in non-survivors). Complete blood count, urinalysis, biochemical analysis, coagulation testing, and measurement of anti-SARS-CoV-2 IgM/IgG were carried out in all patients immediately upon the admission to intensive care unit.Results. Risk factors for death in severe COVID-19 at the admission to intensive care unit were arterial hypertension, chronic heart failure, peripheral atherosclerosis, impaired renal homeostasis (reduced glomerular filtration rate, elevated serum creatinine and urea, proteinuria, hematuria), augmented fasting blood glucose and lactate, neutrophilia (in men), lymphopenia and increased neutrophil-to-lymphocyte ratio (in women), and decreased IgM/IgG to SARS-CoV-2 (in women).Conclusion. We found both independent and gender-specific risk factors for death due to COVID-19.

Evaluation of Regional Lung Function in Pulmonary Fibrosis with Xenon-129 MRI.

Idiopathic pulmonary fibrosis, a pattern of interstitial lung disease, is often clinically unpredictable in its progression. This paper presents hyperpolarized Xenon-129 chemical shift imaging as a noninvasive, nonradioactive method of probing lung physiology as well as anatomy to monitor subtle changes in subjects with IPF. Twenty subjects, nine healthy and eleven IPF, underwent HP Xe-129 ventilation MRI and 3D-SBCSI. Spirometry was performed on all subjects before imaging, and DLCO and hematocrit were measured in IPF subjects after imaging. Images were post-processed in MATLAB and segmented using ANTs. IPF subjects exhibited, on average, higher Tissue/Gas ratios and lower RBC/Gas ratios compared with healthy subjects, and quantitative maps were more heterogeneous in IPF subjects. The higher ratios are likely due to fibrosis and thickening of the pulmonary interstitium. T2* relaxation was longer in IPF subjects and corresponded with hematocrit scores, although the mechanism is not well understood. A lower chemical shift in the red blood cell spectroscopic peak correlated well with a higher Tissue/RBC ratio and may be explained by reduced blood oxygenation. Tissue/RBC also correlated well, spatially, with areas of fibrosis in HRCT images. These results may help us understand the underlying mechanism behind gas exchange impairment and disease progression.

Zinc supplementation as an adjunct therapy for COVID-19: Challenges and opportunities.

An outbreak of a novel coronavirus (COVID‐19 or 2019‐CoV) infection has posed significant threats to international health and the economy. Patients with COVID‐19 are at risk of cytokine storm, acute respiratory distress syndrome (ARDS), reduced blood oxygenation, mechanical ventilation, and a high death rate. Although recent studies have shown remdesivir and dexamethasone as treatment options, there is an urgent need to find a treatment to inhibit virus replication and to control the progression of the disease. Essential biometal zinc has generated a lot of excitement as one of the promising candidates to reduce the severity of COVID‐19 infection. Several published observations outlined in the review are the reasons why there is a global enthusiasm that zinc therapy could be a possible therapeutic option. However, the biggest challenge in realising the therapeutic value of zinc is lack of optimal treatment modalities such as dose, duration of zinc supplementation and the mode of delivery. In this review, we discuss the regulatory mechanism that hinges upon the bioavailability of zinc. Finally, we propose that intravenous zinc could circumvent the confounding factors affecting the bioavailability of zinc and allow zinc to achieve its therapeutic potential. If successful, due to advantages such as lack of toxicity, low cost and ease of availability, intravenous zinc could be rapidly implemented clinically.

Betelnut polyphenols provide protection against high-altitude hypoxia in rats

To investigate the protective effects of betelnut polyphenols on the vital organs against high-altitude hypoxia in rats. We compared low-, medium-, and high- dose betelnut polyphenols (400, 800, and 1600 mg/kg, respectively) and rhodiola the effects of against high-altitude hypoxia in Wistar rats. The rats were kept in normal condition and given the drugs daily for 3 days before transfer to a facility at the altitude of 4010 m, where the rats were kept for 5 consecutive days for hypoxic exposure. The rats were then euthanized for measuring arterial blood gas and assessing liver, lung, brain and cardiac pathologies with HE staining. SOD activity, MDA content and GSH content in the organs were measured, and serum levels of inflammatory factors were detected using a protein microarray. Acute exposure to hypoxia significantly reduced blood oxygen saturation of the rats (P < 0.05), caused damages in the liver, lung, brain and myocardium, lowered SOD activity and GSH content and increased MDA content in the vital organs, and increased serum levels of TIMP-1, MCP-1, ICAM-1, and L-selectin (P < 0.05). Treatment with betelnut polyphenols significantly improved blood oxygen saturation, alleviated organ damages, decreased MDA content and increased SOD activity and GSH content in the tissues, and significantly lowered serum levels of inflammatory cytokines in rats with acute exposure to high-altitude hypoxia (P < 0.05). Betelnut polyphenols provides protection of the vital organs against acute high-altitude hypoxia in rats by enhancing the antioxidant capacity and reducing inflammatory response.

Elevated inflammatory responses and targeted therapeutic intervention in a preclinical mouse model of ataxia-telangiectasia lung disease

Ataxia-telangiectasia (A-T) is an autosomal recessive, multisystem disorder characterized by cerebellar degeneration, cancer predisposition, and immune system defects. A major cause of mortality in A-T patients is severe pulmonary disease; however, the underlying causes of the lung complications are poorly understood, and there are currently no curative therapeutic interventions. In this study, we examined the lung phenotypes caused by ATM-deficient immune cells using a mouse model of A-T pulmonary disease. In response to acute lung injury, ATM-deficiency causes decreased survival, reduced blood oxygen saturation, elevated neutrophil recruitment, exaggerated and prolonged inflammatory responses and excessive lung injury compared to controls. We found that ATM null bone marrow adoptively transferred to WT recipients induces similar phenotypes that culminate in impaired lung function. Moreover, we demonstrated that activated ATM-deficient macrophages exhibit significantly elevated production of harmful reactive oxygen and nitrogen species and pro-inflammatory cytokines. These findings indicate that ATM-deficient immune cells play major roles in causing the lung pathologies in A-T. Based on these results, we examined the impact of inhibiting the aberrant inflammatory responses caused by ATM-deficiency with reparixin, a CXCR1/CXCR2 chemokine receptor antagonist. We demonstrated that reparixin treatment reduces neutrophil recruitment, edema and tissue damage in ATM mutant lungs. Thus, our findings indicate that targeted inhibition of CXCR1/CXCR2 attenuates pulmonary phenotypes caused by ATM-deficiency and suggest that this treatment approach represents a viable therapeutic strategy for A-T lung disease.

In This Issue

In This Issue

Remote photonic sensing of blood oxygen saturation via tracking of anomalies in micro-saccades patterns.

Speckle pattern analysis has been found by many researchers to be applicable to remote sensing of various biomedical parameters. This paper shows how analysis of dynamic differential speckle patterns scattered from subjects' sclera illuminated by a laser beam allows extraction of micro-saccades movement in the human eye. Analysis of micro-saccades movement using advanced machine learning techniques based on convolutional neural networks offers a novel approach for non-contact assessment of human blood oxygen saturation level (SpO2). Early stages of hypoxia can rapidly progress into pneumonia and death, and lives can be saved by advance remote detection of reduced blood oxygen saturation.

An adverse outcome pathway for lung surfactant function inhibition leading to decreased lung function

Inhaled substances, such as consumer products, chemicals at the workplace, and nanoparticles, can affect the lung function in several ways. In this paper, we explore the adverse outcome pathway (AOP) that starts when inhaled substances that reach the alveoli inhibit the function of the lung surfactant, and leads to decreased lung function. Lung surfactant covers the inner surface of the alveoli, and regulates the surface tension at the air–liquid interface during breathing. The inhibition of the lung surfactant function leads to alveolar collapse because of the resulting high surface tension at the end of expiration. The collapsed alveoli can be re-opened by inspiration, but this re-opening causes shear stress on cells covering the alveoli. This can damage the alveolar-capillary membrane integrity, allowing blood components to enter the alveolar airspace. Blood components, such as albumin, can interact with the lung surfactant and further inhibit its function. The collapse of the alveoli is responsible for a decrease in the surface area available for blood oxygenation, and it reduces the volume of air that can be inhaled and exhaled. These different key events lead to decreased lung function, characterized by clinical signs of respiratory toxicity and reduced blood oxygenation. Here we present the weight of evidence that supports the AOP, and we give an overview of the methods available in vitro and in vivo to measure each key event of the pathway, and how this AOP can potentially be used in screening for inhalation toxicity.

The effects of elevated potassium, acidosis, reduced oxygen levels, and temperature on the functional properties of isolated myocardium from three elasmobranch fishes: clearnose skate (Rostroraja eglanteria), smooth dogfish (Mustelus canis), and sandbar shark (Carcharhinus plumbeus).

Elevated plasma potassium levels (hyperkalemia), reduced plasma pH (acidosis), reduced blood oxygen content, and elevated temperatures are associated with species-specific rates of at-vessel and post-release mortality in elasmobranch fishes. The mechanism linking these physiological disturbances to mortality remains undetermined however, and we hypothesize that the proximate cause is reduced myocardial function. We measured changes in the functional properties of isolated ventricular myocardial strips from clearnose skate (Rostroraja eglanteria), smooth dogfish (Mustelus canis), and sandbar shark (Carcharhinus plumbeus) when subjected to the following stressors (both in isolation and in combination): hyperkalemia (7.4mMK+), acidosis (from 7.9 to 7.1), and reduced oxygen (to 31% O2 saturation) applied at temperatures 5°C above and below holding temperatures. We selected these species based on phylogenetic distance, diverse routine activity levels, and their tolerance to capture and transport. Stressors had a few significant species-specific detrimental impacts on myocardial function (e.g., a 33-45% decrease in net force under acidosis + low O2). Net force production of myocardial strips from clearnose skate and smooth dogfish approximately doubled following exposure to isoproterenol, demonstrating that these species possess beta-adrenergic receptors and that their stimulation could provide a mechanism for preservation of cardiac function during stress. Our results suggest that disruption of physiological homeostasis associated with capture may fatally impair cardiac function in some elasmobranch species, although research with more severe stressors is needed.

Progressive Hypoxia: A Pivotal Pathophysiologic Mechanism of COVID-19 Pneumonia

Progressive Hypoxia: A Pivotal Pathophysiologic Mechanism of COVID-19 Pneumonia

Disease severity-related alterations of cardiac microRNAs in experimental pulmonary hypertension.

Right ventricular (RV) failure is the primary cause of death in pulmonary arterial hypertension (PAH). We hypothesized that heart‐relevant microRNAs, that is myomiRs (miR‐1, miR‐133a, miR‐208, miR‐499) and miR‐214, can have a role in the right ventricle in the development of PAH. To mimic PAH, male Wistar rats were injected with monocrotaline (MCT, 60 mg/kg, s.c.); control group received vehicle. MCT rats were divided into two groups, based on the clinical presentation: MCT group terminated 4 weeks after MCT administration and prematurely terminated group (ptMCT) displaying signs of terminal disease. Myocardial damage genes and candidate microRNAs expressions were determined by RT‐qPCR. Reduced blood oxygen saturation, breathing disturbances, RV enlargement as well as elevated levels of markers of myocardial damage confirmed PH in MCT animals and were more pronounced in ptMCT. MyomiRs (miR‐1/miR‐133a/miR‐208a/miR‐499) were decreased and the expression of miR‐214 was increased only in ptMCT group (P < 0.05). The myomiRs negatively correlated with Fulton index as a measure of RV hypertrophy in MCT group (P < 0.05), whereas miR‐214 showed a positive correlation (P < 0.05). We conclude that the expression of determined microRNAs mirrored the disease severity and targeting their pathways might represent potential future therapeutic approach in PAH.

Neural Signatures of Memory Encoding in Schizophrenia Are Modulated by Antipsychotic Treatment

There is no pharmacological treatment to remediate cognitive impairment in schizophrenia (SZ). It is imperative to characterize underlying pathologies of memory processing in order to effectively develop new treatments. In this longitudinal study, we combined functional magnetic resonance imaging during a memory encoding task with proton MR spectroscopy to measure hippocampal glutamate + glutamine (Glx). Seventeen SZ were scanned while unmedicated and after 6 weeks of treatment with risperidone and compared to a group of matched healthy controls (HC) scanned 6 weeks apart. Unmedicated patients showed reduced blood oxygen level dependent (BOLD) response in several regions, including the hippocampus, and greater BOLD response in regions of the default mode network (DMN) during correct memory encoding. Post hoc contrasts from significant group by time interactions indicated reduced hippocampal BOLD response at baseline with subsequent increase following treatment. Hippocampal Glx was not different between groups at baseline, but at week 6, hippocampal Glx was significantly lower in SZ compared to HC. Finally, in unmedicated SZ, higher hippocampal Glx predicted less deactivation of the BOLD response in regions of the DMN. Using 2 brain imaging modalities allowed us to concurrently investigate different mechanisms involved in memory encoding dysfunction in SZ. Hippocampal pathology during memory encoding stems from decreased hippocampal recruitment and faulty deactivation of the DMN, and hippocampal recruitment during encoding can be modulated by antipsychotic treatment. High Glx in unmedicated patients predicted less deactivation of the DMN; these results suggest a mechanism by which faulty DMN deactivation, a hallmark of pathological findings in SZ, is achieved.

The risk of bronchial asthma exacerbations among smokers with asthma-chronic obstructive pulmonary disease overlap after inpatient treatment

To assess the risk of exacerbations of bronchial asthma (BA) in smoking patients with the asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) after inpatient treatment. 36 smokers with ACO (main group) and 36 non-smoking patients (control group) with severe or moderate exacerbation of bronchial asthma were examined. Assessment of the severity of exacerbation of BA before treatment, levels of control and risk of exacerbations of BA after treatment was determined according to the Federal clinical guidelines for the diagnosis and treatment of BA (2016). Spirometry, monitoring of blood oxygenation using transcutaneous spectral pulse oximetry and enzyme immunoassay for determination of matrix metalloproteinases 9 were performed. Smoking experience, smoking index and pack/years index were taken into account in patients with ACO. The carboxyhaemoglobin level was analyzed by the carbon monoxide fraction in the exhaled air. For the first time in patients with the ACO, the ability of heavy tobacco smoking and associated decrease in blood oxygenation to potentiate the negative impact of other predictors on the risk of exacerbations of the underlying disease was revealed. In smoking patients with the ACO, for the first time, a direct association of higher levels of matrix metalloproteinases 9 (measured before inpatient treatment) with such a predictor of the risk of further exacerbations of the disease as more frequent detection of symptoms of uncontrolled BA was revealed. In non-smoking patients with BA, a direct relationship between increased sputum secretion and eosinophilia of blood and/or sputum (a predictor of exacerbation of BA) and the relative duration of episodes of decreased blood oxygenation was established. It was found that intensive and prolonged smoking increases the duration and reduces the effectiveness of inpatient treatment of patients with ACO, contributing to the preservation of air traps and low (forced expiratory volume in 1 second 60%) ventilation capacity of the lungs with the persistence of moderately reduced blood oxygenation; the risk of further exacerbations of BA in this phenotype of patients is significantly higher than in non-smoking patients with BA without combination with COPD.

Interspecific Differences in the Metabolic Rate, Gill Dimension and Hematology of Fish in an Amazonian Floodplain Lake

It has been hypothesized that respiratory physiology in fish is closely associated with ecological traits. Therefore, data on gill morphometrics (lamellae frequency, gill surface area and barrier thickness), metabolic rate (oxygen consumption) and blood oxygen capacity (hematology) were analyzed in several fish, including benthic, bentho-pelagic and pelagic species collected in an Amazon floodplain lake. Similar to other teleostean species, the 2nd and 3rd gill arches have numerous large filaments in both pelagic and benthic species, as these characteristics tend to increase the gill surface area. A large gill area (4 to 7 cm2 g-1, mass-specific) is associated with a high (100 to 300 mg O2 h-1 kg-1) routine oxygen consumption rate and has been observed in active pelagic swimmers, such as Cichla monoculus and Pygocentrus nattereri. Benthic dwelling fish (e.g., Pterygoplichthys pardalis and Sorubim lima) have low metabolic rates (20 to 50 mg O2 h-1 kg-1), small gill dimensions (2 to 3 cm2 g-1, mass-specific), low hemoglobin levels (3 to 5 g dL-1), reduced numbers of circulating red blood cells (1 to 2 Í106 mm-3) and low hematocrit values (25 to 35%) compared to pelagic species. These results demonstrated that pelagic fish have high routine oxygen consumption rates compatible with their large gill surface area and high blood oxygen capacity, whereas benthic species have low metabolic rates, small gill dimensions and reduced blood oxygen capacity.

Obstructive sleep apnea syndrome and cognitive impairment

Sleep-disordered breathing is associated with sleep fragmentation and reduced blood oxygenation due to apnea and hypopnea episodes. Multiple studies indicate that obstructive sleep apnea syndrome (OSAS) can have negative impact on cognitive functioning, primarily executive functions, attention, and episodic memory. The attention is also focused on cognition in patients with neurologic and psychiatric comorbidities. There are different explanatory models, which show the mechanisms of OSAS influence on cognition. However, it is still unclear how the initial severity of the disease and clinical outcomes interrelate, and which factors play role in the compensation of cognitive dysfunction. Better understanding of these issues is crucial for the prevention of cognitive impairment and rehabilitation of cognitive functioning.

Fear conditioning and extinction in alcohol dependence: Evidence for abnormal amygdala reactivity.

Fear conditioning and extinction (FCE) are vital processes in adaptive emotion regulation and disrupted in anxiety disorders. Despite substantial comorbidity between alcohol dependence (ALC) and anxiety disorders and reports of altered negative emotion processing in ALC, neural correlates of FCE in this clinical population remain unknown. Here, we used a 2-day fear learning paradigm in 43 healthy participants and 43 individuals with ALC at the National Institutes of Health. Main outcomes of this multimodal study included structural and functional brain magnetic resonance imaging, clinical measures, as well as skin conductance responses (SCRs) to confirm differential conditioning. Successful FCE was demonstrated across participants by differential SCRs in the conditioning phase and no difference in SCRs to the conditioned stimuli in the extinction phase. The ALC group showed significantly reduced blood oxygenation level-dependent responses in the right amygdala during conditioning (Cohen's d = .89, P(FWE) = .037) and in the left amygdala during fear renewal (Cohen's d = .68, P(FWE) = .039). Right amygdala activation during conditioning was significantly correlated with ALC severity (r = .39, P(Bonferroni) = .009), depressive symptoms (r = .37, P(Bonferroni) = .015), trait anxiety (r = .41, P(Bonferroni) = .006), and perceived stress (r = .45, P(Bonferroni) = .002). Our data suggest that individuals with ALC have dysregulated fear learning, in particular, dysregulated neural activation patterns, in the amygdala. Furthermore, amygdala activation during fear conditioning was associated with ALC-related clinical measures. The FCE paradigm may be a promising tool to investigate structures involved in negative affect regulation, which might inform the development of novel treatment approaches for ALC.

Temporal Characteristics of Priming of Attention Shifts Are Mirrored by BOLD Response Patterns in the Frontoparietal Attention Network.

Priming of attention shifts involves the reduction in search RTs that occurs when target location or target features repeat. We used functional magnetic resonance imaging to investigate the neural basis of such attentional priming, specifically focusing on its temporal characteristics over trial sequences. We first replicated earlier findings by showing that repetition of target color and of target location from the immediately preceding trial both result in reduced blood oxygen level-dependent (BOLD) signals in a cortical network that encompasses occipital, parietal, and frontal cortices: lag-1 repetition suppression. While such lag-1 suppression can have a number of explanations, behaviorally, the influence of attentional priming extends further, with the influence of past search trials gradually decaying across multiple subsequent trials. Our results reveal that the same regions within the frontoparietal network that show lag-1 suppression, also show longer term BOLD reductions that diminish over the course of several trial presentations, keeping pace with the decaying behavioral influence of past target properties across trials. This distinct parallel between the across-trial patterns of cortical BOLD and search RT reductions, provides strong evidence that these cortical areas play a key role in attentional priming.

Reduced blood oxygen levels induce changes in low-threshold motor unit firing that align with the individual's tolerance to hypoxia.

This study aimed to quantify how acute hypoxia impacts firing characteristics of biceps brachii motor units (MUs) during sustained isometric elbow flexions. MU data were extracted from surface electromyography (EMG) during 25% maximal voluntary contractions (MVC) in 10 healthy subjects (age 22 ± 1 yr). Blood oxygen saturation (SpO2) was then stabilized at 80% by reducing 1% of the fraction of inspired oxygen every 3 min for 35 min. MU data were once again collected 1 h and 2 h following the 35-min desaturation phase. Although MVC remained unaffected during 2 h of 80% SpO2, subject-specific changes in MU firing rate were observed. Four of 10 subjects exhibited a decrease in firing rate 1 h postdesaturation (12 ± 11%) and 2 h postdesaturation (16 ± 12%), whereas 6 of 10 subjects exhibited an increase in firing rate 1 h (9 ± 6%) and 2 h (9 ± 4%) postdesaturation. These bidirectional changes in firing rate were strongly correlated to the desaturation phase and the subjects' SpO2 sensitivity to oxygen availability, where subjects who had decreased firing rates reached the target SpO2 20 min into the desaturation phase (R2 = 0.90-0.98) and those who had increased firing rates reached the target SpO2 35 min into the desaturation phase (R2 = 0.87-0.98). It is unlikely that a single mechanism accounted for these subject-specific changes in firing rate. Instead, differences in intrinsic properties of the neurons, afferent input to the motoneurons, neuromodulators, and sympathetic nerve activity may exist between groups. NEW & NOTEWORTHY The mechanisms of compromised motor control when exposed to hypoxia are largely unknown. The current study examined how severe acute hypoxia affects motor unit firing rate during sustained isometric contractions of the bicep brachii. The response to hypoxia was different across subjects, where motor unit firing rate increased for some individuals and decreased for others. This bidirectional change in firing rate was associated with how fast subjects desaturated during hypoxic exposure.

Clinical features and treatment of macrolide-resistant Mycoplasma pneumoniae pneumonia in children

To study the clinical features of macrolide-resistant Mycoplasma pneumoniae pneumonia and its treatment regimens in children. The samples of throat swab or bronchoalveolar lavage fluid were collected from 136 children with Mycoplasma pneumoniae pneumonia. Quantitative real-time PCR was used to detect 2063/2064 A:G mutation in 23S rRNA, and according to such results, the children were divided into drug-resistance group with 81 children and sensitive group with 55 children. The two groups were compared in terms of age composition, respiratory symptoms, extrapulmonary complications, laboratory markers, imaging changes, treatment regimens, and length of hospital stay. Compared with the sensitive group, the drug-resistance group had significantly longer duration of pyrexia and severe fever, a significantly higher percentage of children with reduced blood oxygen saturation, and significantly higher levels of alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) (P<0.05). The conventional azithromycin treatment had a good clinical effect in the sensitive group, while corticosteroid therapy was usually needed in the drug-resistance group. Macrolide-resistant Mycoplasma pneumoniae infection cannot be identified based on a single clinical feature, but prolonged duration of pyrexia and severe fever, reduced blood oxygen saturation, and increased ALT and LDH can suggest the presence of this disease. Azithromycin combined with glucocorticoids may be a good treatment regimen for children with macrolide-resistant Mycoplasma pneumoniae pneumonia.